LIBRARY 

OF  THE 

University  of  California. 


BIOLOGY 

Class       UBH/R^ 


THE  PATHOLOGY 


DIFFERENTIAL    DIAGNOSIS 


INFECTIOUS  DISEASES  OF  ANIMALS 


By  VERANUS  ALVA  MOORE,  B.S.,  M.D. 

Professor  of  Comparative  Pathology,  Bacteriology  and  Meat  Inspection, 

New  York  State  Veterinary  College,  Cornell  University, 

Ithaca,  Nev^'  York. 


With  An  Introduction  by 

DANIEL  ELMER  SALMON,  D.V.M. 

Former  Chief  of  the  Bureau  of  Animal  Industry,  United  States 

Department  of  Agriculture. 


THIRD  EDITION  REVISED  AND  ENLARGED 


WITH   I2ZJLLUSTRATIONS 

'•■'^  OF  THE  \ 

ERSITY  ) 

OF  J 


ITHACA,  N.  Y. 

TAYLOR    &    CARPENTER 

I  908 


6 


K  ' 


^\0^'- 


COl'YRIGHT  I90S 

By  Veranus  Alva  Moore 


PRESS    OF 
JOURNAL   JOB    DEPARTMENT 


TO  DANIEL  ELMER  SALMON 

LARGELY  THROUGH  WHOSE  LABORS  THERE  WAS  ES- 
TABLISHED IN  THE  UNITED  STATES  DEPARTMENT  OF 
AGRICULTURE  THE  BUREAU  OF  ANIMAL  INDUSTRY 
WHICH  HAS  MADE  POSSIBLE  EXTENSIVE  INVESTIGA- 
TIONS INTO  THE  NATURE  OF  EPIZOOTIC  DISEASES 
IN  AMERICA  AND  WHO  FOR  TWENTY-ONE  YEARS 
DIRECTED    THESE    INVESTIGATIONS 

THIS  VOLUME  IS  DEDICATED. 


PREFACE 

The  activity  in  the  study  of  the  infectious  diseases  of  ani- 
mals has  brought  out  many  new  facts  pertaining  to  them  since 
the  pubhcation  of  the  second  edition  of  this  volume.  This 
rapid  increase  of  new  knowledge  and  the  elimination  of  pre- 
viously employed  methods  and  interpretations  render  thepr  e- 
paration  of  a  text-book  suitable  for  student  use  more  and 
more  diflScult. 

In  the  present  revision,  the  general  plan  of  the  arrange- 
ment of  subject  matter  and  the  classification  of  the  diseases 
followed  in  the  previous  editions  have  not  been  changed.  The 
grouping  of  the  infectious  diseases  in  accordance  with  the  clas- 
sification of  their  etiological  factors  is  for  student  purposes  at 
least  proving  to  be  satisfactor}-.  The  rapid  accumulation  of 
literature  on  the  subject  matter  of  this  elementary  work  pre- 
cludes the  pubhcation  of  a  bibliography.  The  appending  of  a 
few  references  after  the  discussion  of  each  disease  to  some  of 
the  more  important  articles  has,  however,  proven  to  be  of 
much  assistance  to  students  just  beginning  the  study  of  in- 
fectious diseases. 

I  desire  to  express  my  appreciation  of  the  kind  reception 
accorded  to  the  second  edition  and  the  helpful  reviews  and 
criticisms  that  it  has  received.  It  is  hoped  that  this  edition 
will  be  of  still  greater  aid  both  to  the  student  and  practitioner 
than  the  former  ones.  My  thanks  are  especially  due  to  Drs. 
S.  H.  Burnett  and  \V.  J.  Taylor  of  this  department  for  helpful 

V.   A.   M. 


PREFACE  TO  THE  FIRST  EDITION 


The  literature  on  infection  and  the  etiology  and  morbid 
anatomy  of  infectious  diseases  of  animals  is  exceedingly  rich 
in  the  results  of  new  discoveries  and  important  investigations. 
However,  students  just  beginning  this  study  and  following  a 
prescribed  curriculum  have  not  the  time  nor  are  they  prepared 
to  read  with  profit  the  detailed  records  of  original  research. 
Such  publications  seem  to  be  better  adapted  for  those  doing 
advanced  or  graduate  work.  Furthermore  many  of  these 
publications  are  out  of  print  and  are  only  available  for  con- 
sultation. F'or  these  reasons  it  is  believed  that  a  volume  con- 
taining the  rudiments  of  the  subject  will  be  of  use  to  the  stu- 
dent and  an  aid  to  the  teacher.  It  is  also  believed  that  such 
a  work  will  be  of  assistance  to  practitioners. 

In  preparing  this  volume  the  aim  has  been  to  bring  to- 
gether in  a  concise  form  the  fundamental  facts  in  the  path- 
ology of  the  more  common  infectious  diseases  of  animals, 
especially  those  existing  in  the  United  States,  with  which 
sanitarians  and  the  practitioners  of  comparative  medicine  must 
contend.  To  this  end  the  current  literature,  the  reports  of 
the  investigations  made  at  various  Institutions  and  Experi- 
ment Stations,  as  well  as  the  standard  works  on  comparative 
pathology  have  been  freely  drawn  upon,  to  all  of  which  full 
acknowledgment  is  hereby  made. 

In  order  to  bring  into  consideration  the  clinical  value  of  a 
knowledge  of  morbid  anatomy  a  few  of  the  symptoms  or  ante- 
mortem  manifestations  have  been  included.  It  is  hoped  that 
this  correlation  of  symptoms  and  lesions  will  stimulate  a  deeper 
interest  in  the  study  of  comparative  pathology  and  thus  render 
it  of  more  permanent  and  practical  value  for  those  entering 
into  the  practice  of  veterinary  medicine. 

In  selecting  the  subject  matter  care  has  been  taken  to 
avoid,  as  far  as  possible,  the  introduction  of  results  concerning 


which  there  are  controversies.  It  has  seemed  best  to  deal 
with  those  facts  about  which  at  the  present  time  there  is  little 
or  no  doubt.  After  the  discussion  of  each  disease  a  few  refer- 
ences to  the  literature  are  appended.  These  are  intended  sim- 
ply to  bring  the  attention  of  the  student  to  a  few  publications 
respecting  the  cause  and  morbid  anatom}^  considered  in  the 
light  of  modern  etiology,  of  the  disease  in  question  and  to  a 
few  articles  containing  the  results  of  original  research. 

In  order  not  to  complicate  or  unnecessarily  expand  this 
text,  a  knowledge  of  general  pathology  and  the  principles  of 
bacteriology  has  been  taken  for  granted. 

The  difficulties  involved  in  the  preparation  of  such  a  text 
are  both  numerous  and  obvious.  The  indication  of  errors  or 
omissions  with  any  other  criticisms  that  will  tend  to  better  the 
volume  and  increase  its  efficiency  for  the  student  will  be 
thankfully  received. 

V.   A.    M. 


TABLE  OF  CONTENTS. 


PAGE 


List  of    Illustrations x 

List  of  Reference  Books i.  xiii 

Introdtction xiv 

CHAPTER  I. 

GENERAL    CONSIDERATION    OF   ETIOLOGY,    INFECTION    AND 
SPECIFIC    INFECTIOUS   DISEASES. 

Etiology I 

Infection 2 

Channels  of  Infection 5 

Wound  infection . 6 

A  specific  infectious  disease 11 

The   differential   characters  of  a  specific  infectious  or   epizootic 

disease 11 

Dissemination  of  infectious  diseases 14 

Cause  of  variations  in  the  course  of  an  infectious  disease 15 

Classification  or  grouping  of  infectious  diseases 16 

Migula's  classification   of  bacteria iS 

CHAPTER    II. 

DISEASES    ATTRIBUTED   TO   WOUND    INFECTION. 

Botryomj'cosis 21 

Omphalophlebitis 25 

White  scours  in   calves 26 

Infectious  suppurative  cellulitis 29 

Fistulous  withers  and  poll-evil 31 

Infectious  mastitis 32 

Miscellaneous  infections 36 

CHAPTER  III. 

DISEASES    CAUSED    BV    BACTERIA — GENUS    STREPTOCOCCUS. 

General  discussion  of  streptococci 38 

Strangles 44 

Equine  contagious  pleuro-pneumonia 49 

Apoplectiform  septicemia  in   chickens 57 

Streptococcus    mastitis 60 

CHAPTER    IV. 

DISEASES    CAUSED    BV     BACTERIA-GENUS   MICROCOCCUS. 

Takosis 6;^ 


Vlll  CONTENTS 

CHAPTER  V. 

DISEASES   CAUSED    BY     BACTERIA— GENUS   BACTERIUM. 

Pasteurelloses 69 

Swine  plague 71 

Hemorrhagic  septicemia  in  cattle 94 

Fowl  cholera 105 

Goose  septicemia in 

Fowl  typhoid 114 

Swine  erysipelas - 123 

Anthrax 129 

Glanders 151 

Tuberculosis 175 

Avian  tuberculosis 203 

Johne's  disease 230 

Ovine  caseous  lymph-adenitis 234 

Asthenia  in  fowls  and  pigeons 243 

Diphtheria  in  calves  and  swine 244 

CHAPTER  VI. 

DISEASES   CAUSED    BY    BACTERIA— GENUS     BACILLUS. 

Hog  cholera 246 

Tetanus 265 

Black  leg 276 

Foot-rot  in  sheep 289 

Miscellaneous  infections  with  bacilli 291 

CHAPTER  VII. 

DISEASES    CAUSED    BY    BACTERIA— FAMILY   SPIRILLACE.^. 

Diseases  of  fowls  caused  by  spirilla 294 

Disease  of  pigs  caused  by  spirochaetes 297 

CHAPTER  VIII. 

DISEASES    CAUSED   BY   FUNGI. 

Actinomycosis 299 

Actinobacillosis 317 

Iveeches 321 

Pneumonomycosis 333 

Epizootic  lymphangitis 342 

Farcy  in  cattle 346 

Mycotic  stomatitis 347 

Blastomycetes,  infection  in  horses 348 

CHAPTER  IX. 

DISEASES    CAUSED   BY    PROTOZOA— GENUS    PIROPLASMA. 

Texas  fever 349 


CONTENTS  IX 

Ictero-heniaturia  in  sheep 3>(>^ 

Equine  malaria 3^9 

Canine  malaria 372 

CHAPTER  X. 

DISEASKS   CAUSED   BV    PROTOZOA — GENUS   AMEBA. 

Infectious  entero-hepatitis  in  turkeys 377 

CHAPTER   XI. 
DISEASES    CAUSED    BV    PROTO/OA— GENUS    TRYPANOSOMA. 

Classification  of  Trypanosoma 39' 

Surra 4oo 

Dourine 4io 

Mai  de  caderas —  423 

Nagana 426 

CHAPTER  XII. 

INFECTIOUS    DISEASES    POR   WHICH    THE   SPECIFIC    CAUSE   IS 

NOT   YET   DETERMINED. 

Rinderpest 43° 

Contagious  pleuro-pneumonia  in  cattle 44' 

Foot  and  mouth  disease 454 

Rabies  .__. 459 

Diphtheria  in  fowls 4'^5 

Influenza 499 

Dog  distemper. 5o6 

Cerebro-spinal  meningitis 5 '4 

Cornstalk  disease  in  cattle 5i7 

Infectious   abortion 523 

Variola  in   animals  529 

Epithelioma   contagiosa 539 

Infective  sarcomata  in   dogs 542 

Fowl   pest 543 

CHAPTER  XIII. 

IMMUNITY     AND    PROTECTIVE    INOCULATION. 

Natural   immunity 545 

Artificial  immunity 547 

Hemolysins 55- 

Protective  inoculation 555 

Prevention 560 

CHAPTER  XIV. 

DISINFECTION. 

Disinfection 5^3 

Disinfection  of  stables 5^7 


X  ILLUSTRATIONS 

ILLUSTRATIONS. 

PLATES. 

Tuberculosis  of  lung,  pig ^ 

Map  showing  Texas  fever  line ^^ 


FIGURES  IN  TEXT. 


1.  Purulent  infiltration 7 

2.  Micrococcus  pyogenes  aureus 8 

3.  Streptococcus  pyogenes 9 

4.  Abscess  in  partially  immunized  rabbit '7 

5.  Streptococcus  of  mastitis 3^ 

6.  Section  of  cow's   udder 34 

7.  Morphology  of  streptococcus 39 

8.  Micrococcus  caprinus ^4 

9.  Bacterium  of  swine  plague 72 

0.  Lung  showing  emphysema  in  interlobular  spaces 78 

1.  Right  lung  of  pig  showing  areas  affected  with  swine  plague _  79 
Portion  of  lung  showing  hemorrhagic  interlobular  infiltration  82 
Hemorrhagic  kidney,  pig ^3 

14.  Hemorrhagic  heart,  cow 

15.  Bacieriuin  sanguinariuni 

16.  Temperature  chart  of  fowls  affected  with  fowl  typhoid  .__ 

17.  Diseased  blood  in  fowl  typhoid "8 

18.  Congested  liver  in  fowl  typhoid i  '9 

19.  Phagocytic  action  of  leucocytes  on  the  red  blood  corpuscles.  120 

20.  Bacterium  of  swine  erysipelas 124 


13 


ICO 


116 


130 
132 


21.  Anthrax  bacteria  from  an  impression  preparation 

22.  Cover-glass  preparation  from  anthrax  blood 

23.  Bacterium  anthracis,  in  blood '3^ 

24.  Nasal  septum  and  turbinated  bone,  glanders 15^ 

25.  Nasal  septum,  advanced  glanders ^57 

26.  Nasal  septum,  showing  scars,  glanders 15S 

27.  Glandered  lung '59 

28.  Section  of  glandered   nodule i^i 

29.  Farcy,  cutaneous  glanders '"2 

30.  Mallein  reaction '"7 

30.  /lacieriuin  tuberculosis '8° 

31.  Lymph  glands  on  side  of  cow's  head iSj 

32.  Dorsal  aspect  of  bovine  lungs '^5 

33.  Bovine  tracheal  and  bronchial  lymph  glands 186 

Posterior  mediastinal  glands ^^7 


34 


35.     Section  of  very  young  tuberch 


ILLUSTRATIONS  XI 

36.  Tuberculous  heart,  cow 190 

37.  Tuberculous  focus  in  cow's  lung 192 

38.  Section  of  tuberculous  lung,   cow 193 

39  Tubercular  pleiira 194 

40.  Tubercles  on   mesentery 195 

41.  Tubercles  on  omentum .._. 196 

42.  Tuberculous  ulcers,  intestine,   cow 197 

43.  Section  of  a  tuberculous  ulcer 198 

44.  Tuberculous  spleen,  pig 201 

45.  Avian  tubercle  bacteria 204 

46.  Culture  of  avian  tubercle 205 

47.  Tuberculous  liver,  fowl 208 

48.  Section  of  a  tubercle,  fowl ._  209 

49.  Tuberculous  mesentery,   fowl 210 

50.  Tuberculous  skin,  fowl 21 1 

51.  Temperature   curve,    tuberculin 221 

52.  Chart  showing  the  effect  of  cold  water  on   temperature 221 

53.  Tuberculin  curve  of  pig 222 

54.  Non-tubercular  temperature  reaction 223 

55.  Chart  showing  tuberculin  reaction 224 

56.  Bacterium  of   Preisz 236 

57.  Caseous  nodules  on  leg  of  rabbit 238 

58.  Lung  of  sheep  with  nodules 239 

59.  Bacillus  of  hog  cholera 249 

60.  Ulcerated  intestine  in  hog  cholera 254 

6t.  Spleen  of  pig,  normal  and  with  hog  cholera 255 

62.  Bacillus  of  tetanus 266 

63.  Bacillus  of  black  leg 278 

64.  Bacillus  of  malignant  edema 287 

65.  Bacillus  necrophorus 290 

66.  Necrotic  area,  liver,  rabbit. 290 

67.  Spirochaett-  anserina 294 

68.  Spirochaetes  from  pig 296 

69.  Ray  fungus 301 

70.  Section  of  young  actinomycotic  growth 302 

71.  Giant  cells  in  actinomycotic  growth 302 

72.  Actinomycosis,  head  of  steer 304 

73.  Young  actinomycotic  growth 306 

74.  Actinomycotic  jaw,  cow 307 

75.  Section  of  actinomycotic  jaw 308 

76.  Actinomycosis  of  upper  jaw 309 

77.  Actinomycosis  in  tongue 310 

78.  Actinomycosis  in  cow's  lung 312 

79.  Actinobacillosis 318 

8c.  Leeches,  lesions  in  lip  of  horse 325 


Xli  ILLUSTRATIONS 

8i.     Various  forms  of  fungus 326 

82.  Leeches,  lesions  in  lip  of  horse 327 

83.  Isolated  nodule  from  lesion 32iS 

84.  Club-like  ends  of  hyphae  fungus,    "leeches" 329 

85.  Section  through  nodule,  "leeches" 330 

86.  Aspergillus  fumigatus 334 

87.  Section  of  lung  showing  aspergillus 336 

88.  Necrosis,  kidney  of  rabbit 340 

89      Piroplas)iia  bigeiniuniii 353 

90.  Coccus  form  of  Piroplasma  higeniinmn 353 

91.  Texas  fever  parasite  in  blood  of  kidney 354 

92.  Coccus  form  of  Texas  fever  parasite  in  kidney 354 

93.  Invasion  of  corpuscles  with /'/Vo/>/fl:5w«<z  bigeininuin 355 

94.  Adult  male  tick,  Boophilus  annulatus 355 

95.  Bull  suffering  from  Texas  fever 356 

96.  Adult  female  tick,  y>'t)0/!'/n7«5  annulatus ^ 357 

97.  Eggs  and  young  tick,  i>\;())!>/?z7«.T  annulatus 35S 

98.  Awcha  nieleagridis 379 

99.  Ceca  of  turkey  with  lesions  of  entero-hepatitis 383 

100.  Cecum  showing  ulcers,  in  entero-hepatitis 384 

lor.   L/iver  of  turkey  affected  with  entero-hepatitis 385 

102.  Early  lesions  in  entero-hepatitis 386 

103.  Trypanosoma  Ihuci — 392 

104.  Trypanoplasina  Jlorrelli 392 

105.  Trvpauosoma  Le7uisi 393 

106.  Map  showing  distribution  of  trypanosomiasis 396 

107.  Trypanosoma  Evansi 4ob 

108.  Trypanosma  cquiperduni 4'2 

109.  Trypanosoma  eqniperdu7n,  dividing 4'3 

1 10.  Negri  bodies 4^2 

111.  Section  of  normal  plexiform  ganglion,  dog 480 

112.  Section  of  plexiform  ganglion  from  a  case  of  rabies 480 

113.  Diphtheria  in  fowls,  eye 4^7 

114.  Diphtheria  in  fowls,   sinus 4^^ 

1 15.  Early  stages  of  diphtheritic  necrosis 4''^9 

116.  Advanced  stage  of  diphtheritic   exudate 49° 

117.  Diphtheritic  exudate,  throat  of  pigeon 492 

118.  Diphtheritic  exudate,  larynx,  fowl 493 

119.  Diphtheritic  exudate,  larynx  and   trachea,  fowl 493 

120.  Sections  of  heads  of  normal  and  diphtheritic   fowls 496 

I2[.   Epithelioma  contagiosa,  fowl 540 

122.  Ehrlich's  figures,  complement 554 

123.  IChrlich's  figures,  various  receptors 554 

124.  Ivhrlich's  figures,  free  receptors 554 

125.  Ehrlich's  figures,   anti-complement 554 


A  LIST  OF  REFERENCE  BOOKS. 


BouLEV  ET   REVNAi..— Nouveau   Dictionaire  pratitiue   de   Medecine  de 

Chirurgie  et  d'Hygiene  Veterinaires. 
Cadeac— Encyclopedic  Veterinaire. 
DiECKERHOFF.— Lehrbuch  der  specielleu  Pathologic   und   Therapie   fiir 

Thicrarztc. 
EllenbKRGER.  vSchuTz  cnd  Baum.— Jahresbericht  liber  die  Leistungen 

auf  dcm  Gebiete  der  Veterinar-Medicin. 
Fleming  —A  manual  of  veterinary  sanitary  science  and  police. 
Friedberger  und  Frohner.— Lehrbuch  der  spezicllcn  Pathologic  u. 

Therapie  der  Haustiere. 
Galtier.— Traite  des  maladies  contagieuses  et  de  la  police  sanitaire  des 

animaux  domestiques. 
Hutyra    uxd    MarEK.— Spezielle      Pathologic     und     Therapie      der 

Haustiere. 
KiTT.— Lehrbuch  der  pathologischen  Anatomic  der  Hausthiere. 
KOLLE   UND  Wassermann.— Handbuch  der  pathogenen   Mikroorgan- 

ismen. 
Law.— Veterinary  Medicine.     (Especially  Vol.  IV.) 
LUBARSCH    und'ostertag.— Ergebnisse  der   allgemeinen   Pathologic 

und  Pathologischen  Anatomic  des  Menschen  und  der  Tiere. 
NOCARD  ET  Leclainche.— Les  maladies  microbiennes  des  animaux. 
OSTERTAG.— Handbook  of  meat  inspection.     Authorized  translation  by 

U.  V.  Wilcox. 
Reynal— Traite  de  la  Police  Sanitaire  des  Animaux  Domestiques. 
Schneidemuhl.— Lehrbuch  der  vergleichenden  Pathologic   und  Ther- 
apie des  Menschen  und  der  Hausthiere. 
Waluey.— The  four  bovine  scourges. 


For  bibliography  on  all  medical  subjects,  see  Index-catalogue  of 
the  Library  of  the  Surgeon-General's  office. 

Annual  reports,  Special  Reports  and  Bulletins  on  Animal  Diseases 
issued  by  the  Bureau  of  Animal  Industry,  U.  S.  Department  of  Agricul- 
ture, Washington,  D.  C. 

Proceedings  of  the  American  Veterinary  Medical  Association. 

The  Bulletins  on  Animal  Diseases  issued  by  the  various  State  Agri- 
cultural Experiment  Stations. 


INTRODUCTION. 

An  elementary  treatise  on  the  patholog}^  of  the  infectious 
diseases  of  animals— a  treatise  that  states  briefly,  clearly  and 
comprehensively  all  that  is  known,  and  excludes  all  that  is 
not  known — has  long  been  needed  not  only  by  the  students 
who  are  beginning  this  interesting  subject,  but  by  members 
of  the  veterinary  profession  who,  as  practitioners,  investigators 
or  teachers,  wish  to  learn  in  the  shortest  time  the  present  con- 
dition of  our  knowledge.  A  work  which  supplies  this  need 
will  be  welcomed  and  appreciated. 

There  are  few  subjects  more  important  to  Americans  than 
a  thorough  comprehension  of  the  infectious  diseases  of  ani- 
mals. An  enormous  amount  of  money  is  invested  in  the 
domesticated  animals  in  the  United  States,  and  the  security  of 
this  investment  depends  very  largely  upon  our  ability  to  pro- 
tect these  animals  from  infectious  diseases.  There  are  many 
diseases  of  this  class  which  spread  among  animals  as  smallpox, 
bubonic  plague  or  cholera  spreads  among  mankind;  and  it  re- 
quires a  thorough  knowledge  of  all  the  characteristics  of  such 
diseases  to  guard  against  them,  to  recognize  them  when  they 
appear  or  to  control  them. 

For  a  period  already  too  long,  exact  knowledge  of  these 
diseases  has  been  confined  to  a  comparatively  small  number  of 
men;  but  with  the  great  property  interests  at  stake  it  is  ex- 
tremely desirable  that  this  information  should  be  distributed, 
that  not  only  responsible  officials  but  every  practitioner  should 
share  it.  With  not  far  from  three  thousand  million  dollars 
worth  of  farm  animals  in  this  country,  and  with  a  single  dis- 
ease that  sometimes  destroys  a  hundred  million  dollars  worth 


INTRODUCTION  XV 

of  property  in  a  year,  it  is  not  difficult  to  see  the  value  of  that 
precise  knowledge  which  is  required  to  deal  promptly  and 
efficiently  vv'ith  these  plagues. 

It  is  a  narrow  and  incorrect  view  to  hold  that  the  farmer 
who  owns  these  animals  is  the  only  one  who  suffers  from  the 
ravages  of  the  diseases  which  destroy  them.  Animal  pro- 
ducts constitute  a  large  part  of  the  national  food  supply.  If 
this  food  supply  is  diminished,  made  dearer  and  more  difficult 
to  obtain,  want,  misery,  disease  and  death  among  mankind 
increase.  At  first  the  effects  of  a  scarcity  of  the  food  supply 
ma3^  be  almost  inappreciable  and  felt  only  by  the  verv  poor; 
but  as  the  conditions  of  famine  are  approached,  suffering  is 
multiplied  and  intensified  until  whole  communities  are  pros- 
trated or  destroyed.  An  abundant  supply  of  wholesome  and 
nutritious  food  is  therefore  an  essential  condition  of  the  wel- 
fare and  prosperity  of  the  people. 

The  great  commercial  operations  of  nations  also  depend 
to  a  great  extent  upon  the  good  condition  of  animals.  When 
all  of  the  horses  are  disabled  by  an  epizootic,  as  they  have 
been  on  rare  occasions  by  influenza,  the  delivery  of  purchased 
goods  has  nearly  ceased,  the  shipments  of  flour,  iron,  machin- 
ery and  other  products  have  been  temporarily  arrested  and 
business  has  been  almost  at  a  standstill.  Again,  it  should  be 
remembered  that  we  export  annually  from  the  United  States 
forty  million  dollars  worth  of  live  animals,  one  hundred  mil- 
lion dollars  worth  of  meats,  fifty-five  million  dollars  worth  of 
lard,  tallow  and  other  animal  fats,  and  nine  million  dollars 
worth  of  dairy  products.  Let  this  traffic  be  stopped  by  the 
shortage  of  supplies  or  by  prohibitive  orders  of  other  nations 
on  account  of  the  unrestrained  prevalence  of  infectious  dis- 
eases, and  the  earnings  of  steamships,  and  railroads,  and 
banks,  and  commission  houses,  are  at  once  diminished;  men 


XVI  INTRODUCTION 

employed  in  these  enterprises  are  discharged,  and  in  innumer- 
erable  ways  the  welfare  of  people  who  have  no  part  in  the 
ownership  of  any  of  these  animals  or  their  products  is  affected. 

Finally  the  most  serious  of  all  is  the  case  in  which  the 
animal  plague,  in  addition  to  being  destructive  to  animal  life, 
is  communicable  to  and  fatal  to  man,  as  is  true  of  anthrax, 
rabies  and  tuberculosis.  Such  diseases  destroy  property,  dis- 
turb business,  lessen  the  food  supply,  and  directly  threaten 
human  life.  What  more  is  needed  to  impress  upon  the  reader 
the  supreme  importance  of  studying  and  understanding  the  in- 
fectious diseases  of  animals  ? 

The  pathology  of  these  diseases  is  in  itself  a  large  subject. 
Investigations  concerning  it  have  extended  over  more  than  a 
century  of  time  and  the  literature  of  the  subject  is  enormous. 
To  concentrate  this  knowledge,  to  select  the  truth  and  discard 
the  errors,  and  to  develop  a  concise  and  systematic  treatise  is 
a  task  of  great  magnitude  and  one  which  has  required  much 
labor  and  thought.  The  writer  has  not  seen  the  manuscript, 
but,  from  his  long  and  intimate  acquaintance  with  the  author, 
he  feels  sure  that  the  work  has  been  patiently,  carefully,  intelli- 
gently and  thoroughly  done,  and  that  it  will  be  favorably 
received. 

D    E.  Salmon. 


CHAPTER   I. 

GENERAL    CONSIDERATION    OF    ETIOLOGY,     INFECTION 
AND    SPECIFIC    INFECTIOUS    DISEASES. 


§  I.  Etiology.  The  development  of  the  science  of  bac- 
teriology, together  with  a  knowledge  of  the  parasitic  protozoa, 
has  already  demonstrated  that  a  large  number  of  the  infectious 
diseases  are  the  direct  result  of  the  invasion  of  the  animal  body 
by  certain  species  of  microorganisms.  A  specific  etiology 
which  teaches  that  for  each  of  the  various  epizootics  we  have  a 
single,  definite  cause  has  become  recognized  and  been  accepted 
by  all  pathologists.  Although  there  are  a  number  of  distinct 
diseases  for  which  such  a  specific  agent  has  not  been  found, 
the  evidence  in  the  very  nature  of  the  maladies  is  conclusive 
that  for  each  of  these  such  an  etiological  factor  exists. 

In  studying  the  pathology  of  infectious  diseases  the  idea 
of  a  definite  and  adequate  cause  should  be  kept  in  mind.  It  is 
no  longer  justifiable  to  attribute  them  to  an  unfavorable  en- 
vironment, poor  hygiene,  or  improper  sanitation,  conditions 
which  may  aid  the  specific  cause  but  which  cannot  supplant 
it.  It  is  often  a  troublesome  task  to  differentiate  between  the 
morbid  affections,  often  fatal  in  their  results,  brought  about  by 
improper  care  and  food,  and  the  maladies  dependent  upon  a 
specific  cause.  The  reason  why  many  of  the  former  theories 
accepted  unsanitary  conditions,  certain  kinds  of  food  or  other 
similar  agencies  as  the  etiology  of  distinct,  infectious  diseases, 
is  found  in  the  fact  that  the  infectious  microorganisms-  were 
and  still  are  often  transmitted  to  the  individual  through  such 
channels.  It  is  important,  therefore,  that  the  limitations  of 
both  the  exciting  cause  and  the  environment  should  be  fully 
taken  into  account.  Although  for  certain  diseases  such  as 
rinderpest  we  do  not  know  just  what  the  specific  cause    is, 


2  ETIOLOGY 

the  fact  that  its  location  in  the  body  of  the  diseased  animal 
is  known,  that  with  the  morbid  tissues  the  disease  can  be 
produced  in  healthy  animals  and  that  without  this  definite 
infection,  no  matter  what  the  conditions  are,  the  malady  can- 
not be  made  to  develop,  argues  against  extraneous  conditions 
as  exciting  causes. 

The  mystery  which  formerly  surrounded  the  origin,  the 
course  and  the  disappearance  of  animal  plagues  has  in  a  large 
degree  been  cleared  away  ;  and  in  its  place  we  are  confronted 
with  the  problems  involved  in  the  life  history  and  the  possi- 
bilities of  invading  microorganisms.  In  fact  during  the  last 
few  years  the  biological  sciences  have  been  brought  into  im- 
mediate use  by  the  pathologists.  Etiology  has  become  per- 
manently linked  to  microbiology  so  that  in  seeking  for  the 
specific  cause  of  an  infectious  disease  we  look  for  some  species 
of  organic  life  which  may  belong  either  to  the  animal  or  to  the 
vegetable  kingdom.  The  fact  that  certain  microscopic  animals 
and  plants  have  become,  if  they  were  not  in  the  beginning, 
parasitic  on  larger  and  higher  forms  of  life  has  long  been 
recognized  ;  but  the  idea  came  later,  that  the  various  infections 
giving  rise  to  a  wide  series  of  phenomena,  known  as  symp- 
toms and  morbid  anatomy,  were  actually  and  simply  the  results 
of  the  invasion  of  the  individual  with  living  microscopic  plants 
(bacteria)  or  animals  (protozoa).  It  is  likewise  true  that  for 
many  of  the  disorders  consisting  of  changes  recognized  in  the 
terms  of  general  pathology,  the  cause  may  be  found  in  the 
conditions  of  life  under  which  the  individual  has  been  forced 
to  exist.  Etiology,  therefore,  in  a  broad  sense,  includes  both 
the  infecting  microorganisms  that  produce  the  specific  infectious 
diseases  and  poor  hygienic,  unsanitary  conditions  and  physical 
forces  which  may  produce  non-specific  morbid  changes  often 
sufficient  to  cause  death. 

§  2.  Infection.  The  term  infection  has  come  to  be  gen- 
erally understood  to  mean  the  entrance  into  the  animal  body, 
from  without,  of  living  microorganisms  capable  of  multiplying 
within  the  living  tissues  and  of  producing  in  consequence  of 
this  multiplication  a  local  or  a  general  diseased  condition  and 


INFECTION  3 

possibly  the  death  of  the  individual.  The  invading  microor- 
ganisms may  belong  to  any  one  of  the  three  great  groups  of 
microscopic  life,  namely,  bacteria,  higher  fungi,  and  protozoa. 
It  is  custotuary  and  convenient,  if  not  altogether  logical,  to 
limit  the  term  microorganisms  to  these  forms,  excluding  alto- 
gether the  entozoa  and  other  animal  parasites,  most  of  which 
are  not  microscopic  in  size. 

A  diseased  condition  produced  by  substances  not  capable 
of  reproducing  themselves,  as,  for  example,  organic  or  inor- 
ganic chemical  compounds,  is  an  intoxicative  process.  In  an 
infection,  the  immediate  cause  of  the  symptoms  and  morbid 
changes  in  the  tissues  is  an  intoxication  due  to  the  action  of 
the  metabolic  products  (toxins)  of  the  invading  microorgan- 
isms. The  theories  of  their  mechanical  interference  with 
the  normal  functions  of  the  body  or  that  they  absorb  the 
nutriment,  thus  depriving  the  tissues  of  necessary  food,  wait 
for  demonstration.  The  results  of  infection  vary  in  their 
manifestations. 
/  If  the  invading  organisms  remain  at  the  point  of  entrance 

and  produce  local  tissue  changes,  the  condition  is  spoken  of  as 
a  u'Oiind  infection. 

If  the  invading  bacteria  become  widely  distributed  in   the 
circulation  and  tissues,  the  condition  is  known  as  septicemia  or 
bacteremia. 
/  If  the  infecting  bacteria  remain  at  the  point  of  entrance 

^  and  multiply  there,  elaborating  a  toxin  which  is  absorbed  and 
which  causes  symptoms  and  possibly  death,  the  condition  is  a 
toxemia. 

If  there  is  a  febrile  condition,  resulting  from  the  absorp- 
tion of  the  products  of  putrefaction  caused  by  saprophytic 
bacteria,  the  condition  is  called  sapremia. 

If  the  invading  organism  is  one  possessed  of  definite 
pathogenic  properties,  such  as  the  bacterium  of  anthrax,  giv- 
ing rise  to  a  definite  series  of  symptoms  and  lesions,  the  affec- 
tion is  designated  a  specific,  infectious  disease. 

Through  the  agency  of  metastasis,  invading  microorgan- 
isms may  be  carried  from  the  point  of  introduction  to  other 


4  INFECTION 

parts  of  the  body,  where  they  may  become  localized,  multiply, 
and  give  rise  to  any  one  of  many  forms  of  lesions.  It  may 
happen  that  the  point  of  entrance  is  so  obscure  that  the  result- 
ing morbid  changes  are  not  easily  traced  to  an  external 
infection.  There  are  many  illustrations  of  this  in  comparative 
pathology,  such  for  example  as  suppurative  cellulitis.  For 
convenience  in  discussion,  infections  may  be  divided  into  two 
clinical  groups,  namely  :  wound  infections  and  specific  infec- 
tious diseases,  although  in  certain  instances  they  cannot  be 
separated. 

In  arriving  at  a  clear  understanding  of  the  nature  of  infec- 
tions, it  is  well  not  to  be  too  closely  circumscribed  by  classifi- 
cations. It  is  better  to  look  upon  them  as  a  series  of  processes 
going  on  in  the  animal  world  due  to  the  activities  of  infecting 
or  parasitic  microorganisms.  In  other  words,  the  lesions  fol- 
lowing an  infection  are  simply  the  results  of  parasitism. 

In  the  study  of  the  various  forms  of  infection  in  the  lower 
animals,  lesions  have  been  found  to  contain,  apparently  as  their 
causative  factors,  bacteria  which  suggest  at  least  that  certain 
of  the  supposed  saphrophytic  organisms  may,  under  certain 
conditions,  become  parasitic  and  cause  infections  resulting  in 
more  or  less  local  or  general  disturbance.  Many  lesions  seem 
to  be  produced  by  bacteria  which  are  harbored  normally  upon 
the  skin.  When  these  organisms  are  introduced  by  accident 
into  the  living  tissues  they  multiply  and  acquire,  if  they  did 
not  already  possess  it,  the  power  to  produce  tissue  changes. 
We  cannot,  therefore,  dismiss  the  subject  of  infection  without 
a  passing  consideration  of  the  possible  etiological  significance, 
under  certain  conditions,  of  many  species  of  bacteria  ordinarily 
considered  harmless  with  which  the  animal  body  is  constantly 
surrounded.  In  the  search  for  the  cause  of  many  lesions  sup- 
posed from  their  nature  to  be  infectious,  or  in  applying  meth- 
ods for  their  prevention,  it  is  well  to  take  into  consideration  all 
microorganisms  v/hich  might  possibly  be  the  causative  factors 
and  not  limit  the  search  to  the  detection  of  the  already  recog- 
nized pathogenic  species.  Recent  investigations  point  to  the 
conclusion  that  domesticated  animals  frequently  suffer  as  the 


CHANNELS    OF    INFECTION  5 

result  of  the  invasion  of  bacteria  at  present  not  listed  among 
the  pathogenic  microorganisms,  and  what  is  true  in  this  regard 
for  bacteria,  may  be  hypothetically  applied  to  the  higher  fungi 
and  to  the  protozoa. 

§  3.  Channels  of  infection.  There  are  a  number  of 
ways  by  which  microorganisms  may  be  introduced  into  the 
living  tissues  of  the  animal  body.  The  more  common  of  these 
are  as  follows,  namely  : 

1.  Through  the  digestive  tract.  Bacteria  gain  entrance 
into  the  tissues  from  the  digestive  tract  where  they  have  been 
brought  with  the  food  or  water.  It  is  not  clear  in  all  cases 
how  the  invading  organisms  get  into  the  tissues  from  the 
intestine.  It  has  been  demonstrated  that  tubercle  bacteria  will 
pass  through  the  mucosa  with  fat  globules  in  the  process  of 
digestion  and  absorption. 

2.  Through  the  respiratory  tract.  Bacteria  are  taken  into 
the  lungs  with  the  inhaled  atmosphere.  Pulmonary  tuber- 
cular affection  is  often  brought  about  in  this  way. 

3.  Through  abrasions  of  the  skifi  or  intestinal  mucosa. 
The  wide  distribution  of  bacteria  in  nature  renders  it  highly  , 
probable  that  in  all  wounds  of  the  integument  microorganisms 
will  reach  the  fresh  tissues.  They  may  come  from  the  cutting 
or  tearing  implement,  the  particles  of  dirt  which  may  fall  into 
or  upon  the  cut  surface,  or  from  the  ducts  of  the  glands  of  the 
skin  itself.  It  may  happen  that  the  fresh  tissues  thus  exposed 
are  infected  with  one  or  several  species  of  bacteria.  It  may 
be  that  one  or  more  of  these  species  may  be  destroyed  by  the 
living  juices  of  the  body  or  by  the  leucocytes,  or  again  it  is 
possible  that,  from  their  saprophytic  nature,  they  may  not  be 
able  to  multiple  in  this  new  environment ;  in  either  case  the 
infection  is  of  no  significance  and  clinically  would  not  be 
recognized.  It  may  happen  that  only  one  species  of  the  infect- 
ing bacteria  multiplies  and  produces  the  morbid  changes. 
This  would  be  a  single  infection.  If,  however,  two  or  more 
species  cooperate  in  the  production  of  the  lesions,  it  is  called 
a  mixed  infection.     This  term  is  often  used  to  designate  the 


6  WOUND    INFECTION 

condition  where  one  species  may  be  responsible  for  the  tissue 
changes,  although  other  bacteria  are  present  but  only  in  an 
accidental  or  passive  way. 

4.  Through  the  generative  organs.  Infection  of  the 
reproductive  organs  takes  place  in  certain  instances  where  they 
are  the  seat  of  the  disease.  This  is  especially  true  in  case  of 
maladie  du  coit. 

5.  Through  the  agejicy  of  insects.  Some  insects  carry  the 
virus  of  certain  diseases  from  the  infected  and  introduce  it  into 
the  susceptible  individuals.  Thus  the  mosquito  carries  the 
Plasmodium  of  human  malaria,  the  cattle  tick  the  piroplasma 
of  Texas  cattle  fever,  and  flies  are  often  the  introducers  of 
pathogenic  bacteria,  such  as  those  of  anthrax.  In  certain 
instances,  as  with  malaria,  a  part  of  the  life  cycle  of  the  micro- 
organism takes  place  in  the  body  of  the  carrying  insect. 

6.  Transmission  of  the  virus  from  the  parent  to  the  fetus. 
Occasionally  the  young  of  diseased  parents  are  born  infected 
with  the  disease  with  which  one  or  both  of  its  parents  were 
suffering.  In  these  cases  the  specific  bacteria  were  transmitted 
either  from  the  sire  at  the  time  of  coition,  or  later  to  the  fetus 
in  the  uterus  from  the  dam.  It  is  important  not  to  confuse 
these  rare  cases  with  those  in  which  the  offspring  are  born 
uninfected  but  subsequently  contract  the  disease.  Many  of 
the  so-called  hereditary  diseases  are  the  result  of  post-natal 
infection. 

§  4.  \A^ound  Infection.  Wound  infections  are  the  direct 
results  of  the  entrance  of  certain  microorganisms  into  trau- 
matisms and  operative  incisions.  They  fall  very  naturally 
into  two  classes: 

1.  Those  infections  producing  local,  acute  or  more 
chronic  inflammatory  processes  usually  leading  to  suppuration 
and  finally  healing  by  granulation.  This  is  the  form  most 
frequently  encountered  clinically.  The  tissue  changes  are 
those  of  acute  or  chronic  inflammation. 

2.  Infections  which  may  in  the  beginning  appear  like 


WOUND    INFECTION 


the  first  or  cause  so  little  disturbance  as  to  be  unnoticed  at  the 
time,  but  sooner  or  later  result  in  a  local  or  remotely  situated 
lesion  or  lesions.  Frequently  these  are  recognized  as  distinct 
diseases  although  in  some  cases,  such  as  scirrhous  cord,  the 
origin  is  easily  traced  to 
an  operation  where  infec- 
tion was  possible.  This 
group  of  wound  infec- 
tion lesions,  such  as 
scirrhous  cord,  botryo- 
mycosis,  infectious  cel- 
lulitis of  cattle  and  sheep 
and  still  other  disorders 
may  not  appear  to  be 
dependent  upon  wound 
infection  ;  but  the  results 
of  recent  investigations 
suggest  this  as  their  pri- 
mary cause.  These  affec- 
tions will  be  treated  sep- 
a  r  a  t  e  1  y  in  subsequent 
paragraphs  but  their  re- 
lation to  wound  infec- 
tion renders  them  worthy 
of  note  in  this  connec- 
tion. 

In  wound  infection, 
the  invading  organism 
is  not  always  of  the  same 
species.  It  is  because  of 
the  fact  that  wound  in- 
fection lesions  of  a  similar  character  anatomically  may  be 
caused  by  a  number  of  different  bacteria  that  they  cannot  be 
classed  among  the  specific  infectious  diseases.  It  is  observed 
further,  that  in  many  of  these  lesions  two  or  more  species  have 
been  responsible  for  the  results.  There  is  no  symptom,  or 
manifestation  of  tissue  changes,  bv  which   one  can   determine 


Fig.  I.  Wound  infection.  Purulent  in- 
tiltralion  from  the  ivall  of  an  abscess  in 
a  horse  shoiving  the  infiltration  of  the 
intermuscular  tissue  7vith  pus  corpuscles. 
Draii'ing  made  icith  i  inch  ocular  and 
-S  objective. 


8 


WOUND     INFECTION 


the  specificity  of  the  exciting  cause.  If  this  is  done,  it 
requires  a  bacteriological  examination. 

Another  class  of  diseases  that  are  sometimes  called 
wound  infections  should  be  mentioned,  namelj-,  those  specific 
diseases,  such  as  tetanus  and  symptomatic  anthrax,  where  the 
virus  is  supposed  always  to  be  introduced  through  a  wound 
either  in  the  skin  or  mucous  membranes. 

Bacteria  causing  wound  infection.  A  large  number  of 
species  of  bacteria  and   a  few  fungi  are  included  among  the 


Fig    2.      Micrococcus   pyogoies    aureus.      Drai^iug  from    a    cover- 
glass  preparation  of  a  bouillon  culture.      Highly  magnified. 


organisms  which  are  known  to  produce  wound  infections  in 
animals.  Usually,  however,  the  forms  encountered  are  micro- 
cocci, especially  those  belonging  to  the  staphylococcus  group, 
streptococci,  Bacillus  pyogenes  (Bacillus  pyogenes  bovis 
(Grips)  Bacillus  pyogenes  suis  (Kiinnemann)  ),  a  few  other 
bacilli,  especially  those  belonging  to  the  colon  group  and  a 
few  species  of  the  genus  pseudomonas.     Fungi  and   protozoa 


WOUND    INFECTION  9 

are  rarely  found  in  acute  wound  infection  lesions  excepting 
in  specific  diseases  which  they  cause  and  where  their  entrance 
is  through  injuries  or  by  means  of  the  bites  of  insects.  Many 
of  the  specific  pathogenic  bacteria  may  be  introduced  through 
wounds.  As  a  rule,  it  seems  to  be  true  that  in  the  domesti- 
cated animals,  as  in  man,  the  pyogenic  bacteria  are  the  most 
common  and  important  wound  infecting  microorganisms.  In 
open  wounds  these  are,  of  course,  associated  with  a  very  large 
number  of  ordinary  saprophytic  bacteria.  Frequently  in 
closed  lesions  nonpathogenic  organisms  are  present  in  addition 


Vie  3.     Streptococcus  pyogenes.     Draiving  made  front  a  cover-glass 
preparation  from  a  bouillon  culture.     Highly  magnified. 


to  the  seemingly  causative  factors.  It  is  worthy  of  note  that 
it  appears  to  be  impossible  to  predict  from  the  general  charac- 
ter of  the  lesions,  the  kind  of  bacteria  which  are  producing 
them,  except  it  be  in  case  of  infections  like  tuberculosis  or 
actinomycosis.  These  bacteria  are  usually  recognized  without 
trouble  in   cover- glass   preparations   made    from    the    lesions. 


lO  WOUND    INFECTION 

Their  species  can  also  be  easily    determined    by    cultivating- 
them  on  artificial  media/ 

Morbid  anatomy  of  infection.  The  tissue  changes  resulting 
from  an  infection  of  the  body  with  various  microorganisms 
belong  with  those  considered  in  general  pathology  under  the 
headings  of  inflammations,  degenerations,  other  retrograde 
disturbances  and  regenerative  processes.  The  pathology  of 
infection,  therefore,  is  not  a  discussion  of  new  deviations  or 
disturbances  of  cells  and  fibers,  but  rather  a  grouping  or  com- 
bining of  disturbances  already  recognized  as  the  selective 
results  of  the  activities  of  the  particular  invading  organisms. 
Thus  in  ordinary  wound  infections  the  morbid  changes  are 
those  of  an  acute  inflammation  leading  to  suppuration,  necrosis 
or  gangrene  ;  sometimes  they  are  chronic  in  nature,  resulting 
in  formative  changes,  and  again  in  the  various  forms  of  exuda- 
tion. In  other  instances  infection  results  in  hemorrhages  of 
varying  degrees.  Occasionally  the  lesions  may  become  local- 
ized, as  in  pneumonia,  lymphangitis,  intestinal  ulcers,  nephri- 
tis, hepatitis,  splenitis  and  the  like.  The  morbid  anatomy  of 
infection  introduces  few  if  any  changes  not  known  to  general 
pathology.  Because  of  this,  the  emphasis  of  the  pathology  of 
infection  rests  on  the  etiology  and  the  possible  variety  and  dis- 
tribution in  the  body  of  the  tissue  changes.  It  has  been 
shown  that  certain  infections  are  slow  in  bringing  about  tissue 
changes  and  consequently  many  lesions  resulting  from  wound 
infection  may,  when  they  appear,  be  considered  as  distinct 
maladies. 

Preveyition  of  infectioji.  In  surgical  operations,  wound 
infection  may  be  prevented  where  uninfected  lesions  are 
involved  by  disinfecting  the  field  of  operation.  This  is  a  much 
more  difficult  task  than  it  appears.  The  habit  of-  bacteria  of 
growing  down  into  the  hair  follicles,  sweat  glands  and  beneath 
the  dead  epithelial  cells  on  the  surface,  renders  it  necessary 
to  use  a  disinfectant  of  much  penetrating  power  in  order  to 


'For  the  specific  cultural  characters  of  each  of  the  wound   infection 
icteria  the  student  is  referred  to  manuals  of  bacteriology. 


A    SPECIFIC    INFECTIOUS    DISEASE  II 

sterilize  the  skin.      In  case  of  traumatic  infection  the  wound 
itself  must  be  disinfected. 

ij  5.  A  specific  infectious  disease.  A  specific  infec- 
tious disease  is  the  result  of  the  multiplication  within  the  animal^ 
body  of  a  single  species  of  microorganism.  The  lesions  may 
be  local  or  general,  but  the  cause  producing  them  is  always 
the  same.  Thus,  Bacterium  ayithracis  will  produce  a  disease 
which  is  called  anthrax,  no  other  cause  can  produce  it,  and  no 
matter  how  much  the  lesions  may  vary  in  different  individuals 
if  they  are  produced  by  this  species  of  bacteria  the  disease  is 
anthrax.  It  is  clear,  therefore,  that  there  is  no  hard  and  fast 
line  between  a  simple  (single)  wound  infection  and  a  recog- 
nized infectious  or  epizootic  disease,  except  in  the  nature  of  the 
invading  organism.  The  course  of  the  disease  may  vary  in 
different  individuals  and  usually  it  does,  especially  if  in  differ- 
ent species  of  animals.  If  a  man  receives  accidentlly  a  cut 
from  a  knife  with  which  he  is  making  a  post-mortem  on  an 
animal  dead  from  anthrax,  the  lesion  is  liable  to  be  restricted 
to  the  point  of  inoculation,  and  while  it  is  anthrax  (malignant 
pustule)  it  would  often  be  recognized  as  a  simple  wound  infec- 
tion. If  this  accidental  inoculation  should  occur  in  a  guinea 
pig,  the  disease  would  not  be  recognized  as  a  local  lesion  :  but 
the  animal  would  develop  septicemia. 

As  a  class  the  specific  diseases  are  differentiated  from  the 
lesions  known  clinically  as  wound  infections  in  a  number  of 
ways.  The  bacteria  of  the  epizootic  diseases  do  not  ordinarily 
produce  wound  infections  following  accidental  injuries  or  sur- 
gical operations,  although  there  are  exceptions.  Again,  there 
is  usually  a  difference  in  the  mode  of  infection.  The  virus  of 
the  epizootic  diseases  is  ordinarily  introduced  through  the 
digestive  or  respiratory  tract  or  by  means  of  insects,  while  in 
wound  infection  the  virus  is  introduced,  as  the  term  implies, 
through  the  injured  integument  or  mucosa. 

i^  6.     The  differential  characters  of  a    specific   infec- 


'Plants  suffer  from  specific  infectious  diseases   caused   by   bacteria 
and  fungi,  quite  as  much  as  animals. 


12  A   SPECIFIC    INFECTIOUS    DISEASE 

tious  or  epizootic  disease.  It  is  very  important  not  to  mis- 
take for  an  infectious  disease  some  form  of  bodj'  disturbance 
due  to  a  local  cause  or  condition.  Animals  often  suffer  from 
improper  food  and  the  conditions  of  life  under  which  they  are 
compelled  to  live.  It  frequently  happens  that  as  all  ot  the 
animals  in  a  given  herd  are  subjected  to  like  conditions,  a 
number  of  them,  perhaps  all,  will  manifest  very  similar  symp- 
toms and  more  or  less  of  them  die.  Such  an  occurrence  often 
gives  rise  to  the  supposition  that  the  cause  of  death  is  some 
form  of  infection.  Deaths  from  such  causes  or  under  such 
conditions  should  be  carefully  distinguished  from  an  epizootic. 
In  differentiating  a  non-infectious  disorder  from  a  specific  dis- 
ease, it  is  important,  and  usually  sufficient,  to  take  into 
account  the  appended  characteristics  of  an   infectious  disease. 

1.  Cause.  An  infectious  disease  is  caused  by  a  specific 
agent.  This  necessitates  as  the  first  requisite  an  exposure  to 
and  an  infection  with  the  specific  organism. 

2.  Period  of  incubation.  The  infection  must  be  followed 
by  a  certain  period  of  incubation  before  the  development  of 
symptoms.  This  is  the  time  necessary  for  the  invading  micro- 
organism to  become  established  in  the  body  and  to  bring  about 
the  first  symptoms  of  the  disea.se.  The  incubation  period  var- 
ies in  different  diseases,  and  to  a  certain  degree  in  the  same 
disease,  according  to  the  mode  of  infection  and  the  resistance 
of  the  individual.  Usually  the  incubation  period  of  a  given 
disease  is  practically  the  same  for  all  individuals  of  the  same 
species  when  subjected  to  the  same  mode  of  infection.  Ex- 
ceptions, however,  are  not  rare. 

3.  Lesions.  The  morbid  anatomy  of  an  infectious  dis- 
ease is  usually  nearly  the  same  in  animals  suffering  in  the 
same  outbreak,  especially  when  they  were  infected  at  or  about 
the  same  time.  It  is  more  common  for  only  a  few  individuals  in 
a  herd  to  be  infected  in  the  beginning  and  from  these  first  cases 
for  other  animals  to  contract  the  disease.  In  many  epizootics, 
the  disease  appears  in  an  acute  form  in  the  first  animals 
attacked  while  those  infected  later  in  the  course  of  the  outbreak 
suffer  from  a  chronic  form  of  the  affection.     In  other  outbreaks 


DIFFERKNTIATION  1 3 

the  first  cases  are  chronic  in  nature  and  the   later  ones   acute. 

4.  Dnrafio7i.  In  animals,  as  in  man,  most  of  the  infec- 
tious diseases  are  self  limiting,  but,  as  a  rule,  the  percentage 
of  fatal  cases  is  much  larger  among  animals  than  in  the  human 
species.  The  period  of  convalescence  is  not  so  well  marked  in 
the  lower  .«;pecies  as  in  man.  It  frequently  happens  that  the 
course  of  the  disease  is  so  changed  that  an  acute  case  which 
appears  to  recover,  or  at  least  to  pass  into  the  stage  of  con- 
valescence, becomes  chronic  or  subchronic  in  nature  and 
eventually  terminates  in  death.  The  lateness  in  the  develop- 
ment of  the  modified  lesions  often  causes  the  nature  of  the  ter- 
minal disease  to  go  unrecognized. 

5.  Trafismission  by  hioculation.  Finally,  it  is  necessary 
in  making  a  positive  diagnosis  to  find  the  specific  organism, 
or  to  prove  the  transmissibility  of  the  malady  from  the  sick  or 
dead  to  healthy  animals.  The  extent  of  the  spread  of  the 
virus  of  the  disease  through  the  available  channels  for  its  dis- 
semination will  also  aid  in  determining  the  infectious  or  non- 
infectious nature  of  the  malady  in  an  outbreak  among 
animals. 

In  diagnosing  an  epizootic  disease  investigations  have 
shown  that  too  much  reliance  can  not  be  placed  on  the  period 
of  incubation,  or  the  morbid  anatomy.  There  are  many  pos- 
sibilities, therefore,  that  an  erroneous  diagnosis  may  be  made 
when  the  clinical  and  post-mortem  evidences  of  the  disease  are 
alone  considered.  It  has  also  been  determined  that  certain 
non- infectious  disorders  often  assimilate,  in  their  more  general 
manifestations,  the  characters  of  infectious  maladies.  This 
fact  necessitates  much  care  in  the  differentiation  of  outbreaks 
of  animal  diseases. 

The  dietary  and  other  non-infectious  disorders  do  not 
exhibit  definite,  uniform  differential  characters  excepting  per- 
haps in  case  of  those  caused  by  a  few  mineral  poisons  or  by 
eating  certain  plants.  As  examples  of  the.se,  lead  poisoning 
and  the  Pictou  or  Winton  disease  of  horses  and  cattle  caused 
by  eating  a  ragwort  {Stmea'o  jacoboea)  may  be  mentioned. 
The  non-infectious  disorders  are  differentated   from   the   infec- 


14  DISSEMINATION 

tious  ones  largely  by  eliminating  the  characters  of  the   latter 
and  finding,  if  possible,  the  causative  agent. 

The  necessity  for  an  early  and  positive  diagnosis  in  all 
outbreaks  of  epizootic  disease,  is  to  assure  the  enforcement  of 
all  possible  measures  to  prevent  its  spread.  The  essential 
problem  for  the  practitioner  or  sanitarian  in  the  presence  of 
these  diseases,  is  to  restrict  the  number  of  cases  to  the  indi- 
viduals already  infected.  In  order  to  do  this,  it  is  of  much 
importance  that  modified  or  chronic  cases  of  any  infectious 
disease  should  not  escape  detection  if  there  is  danger  of  their 
spreading  the  virus  or  exposing  susceptible  animals. 

§  7.  Dissemination  of  infectious  diseases.  Al- 
though the  discussion  of  the  means  by  which  each  of  the  vari- 
ous diseases  are  disseminated  will  be  found  under  the  considera- 
tions of  the  individual  affections,  it  is  important  to  consider 
the  general  ways  and  means  by  which  these  different  vital 
causative  factors  are  spread  from  an  infected  individual  to  a 
non-infected  one  in  the  same  herd  and  from  one  herd  to 
another.  As  we  understand  them  at  the  present  time,  each 
virus  is  dependent  for  its  perpetuation  upon  its  escape  from 
one  host  (sick  or  dead)  to  another.  As  these  organisms  are 
without  power  of  their  own  for  such  migration,  they  are  depend- 
ent upon  other  forces  and  carriers  to  take  them.  In  finding 
the  cause  of  their  spread,  we  must  consider  first  how  they 
escape  from  the  infected  individual  and  secondly  how  they  are 
carried  rom  one  individual  to  another. 

1.  Escape  of  virus  from  infected  individuals.  The  infect- 
ing organisms  escape  from  the  living  body  either  with  (a)  the 
excreta,  (b)  the  external  discharge  of  ulcers  and  abscesses  or 
both,  and  (c)  the  blood  by  sucking  and  possibly  biting  insects. 
After  the  death  of  the  host  they  can  escape  only  by  the  dis- 
integration of  the  dead  body  or  by  its  being  consumed  by 
other  animals  or  birds.  The  bacteria  of  several  diseases 
can  pass  through  the  digestive  tract  of  such  animals  un- 
injured. 

2.  Dissemination    of   infectiyig    orga7iisms.       Pathogenic 


DISSEMINATION    OF    INFECTION  I5 

bacteria  are  spread  after  they  escape  from  the  body  in  many 
ways,  the  following  being  the  most  common  : 

(a.)      By  direct  contact. 

(b.)  They  are  carried  on  the  hands,  shoes  or  clothing 
of  attendants,  and  on  farm  implements,  such  as  shovels  and 
hoes. 

(c.)  They  are  carried  in  streams  receiving  the  excreta 
or  disintegrating  bodies  of  the  infected. 

(d.)  They  are  scattered  with  the  excreta  of  birds  that 
feed  upon  the  dead  carcasses.  Other  animals,  such  as  dogs 
and  foxes,  are  also  charged  with  the  scattering  of  the  virus  by 
the  same  method. 

(e. )  The  virus  is  often  carried  from  one  herd  to  another 
by  introducing  chronic  cases  or  those  already  infected  in  which 
the  symptoms  have  not  yet  appeared. 

(f.)  Animals  are  often  infected  by  shipping  them  in  cars 
or  crates  that  have  previously  contained  diseased  animals  and 
that  have  not  been  thoroughly  disinfected. 

(g. )  The  pathogenic  protozoa  are  transferred  from 
infected  to  non-infected  individuals  by  means  of  insects.  They 
are  carried  from  place  to  place  in  infected  animals. 

§  8.  Cause  for  the  variations  in  the  course  of  an 
infectious  disease.  It  is  a  recognized  fact  that  there  is  much 
variation  in  the  course  of  infectious  diseases  in  different  epizo- 
otics and  often  marked  individual  variations  occur  in  the  same 
outbreak.  In  explaining  this  interesting  phenomenon,  it  is 
important  to  take  into  account  the  question  of  individual 
resistance  or  immunity,— partial  or  more  complete.  It  was 
found  in  case  of  certain  diseases  that  when  an  individual  was 
partially  immunized  and  then  infected,  that  the  lesions  were 
very  much  modified.  The  teachings  of  a  specific  etiology 
point  to  this  phenomenon  as  a  result  of  certain  biological  or 
vital  differences  existing  either  in  the  parasite  or  in  the  host, 
possibly  in  both.  The  results  of  the  investigations  already 
made  along  this  line  suggest  as  a  probable  explanation,   that 


l6  CAUSE    FOR    VARIATION 

the  course  of  the  disease  varies  on  the  one  side  with  the  resist- 
ance of  the  host  and  on  the  other  with  the  degree  of  virulence 
of  the  infecting  microorganism.  This  has  been  expressed  in 
the  formula 

-^ 

in  which  D  =  the  disease,  V  -  -  the  virulence  of  the  infecting 
organism,  and  R  ^-  the  resistance  of  the  host  or  the  individual 
attacked.  As  V  or  R  change  the  disease  is  modified.  For 
example,  rabbits  that  are  partially  immunized  against  swine 
plague  bacteria,  when  inoculated  with  a  virulent  culture  of 
that  organism,  will  live  for  several  days  and  perhaps  for  weeks, 
and  then  die  of  peritonitis,  pleuritis  or  extensive  pus  forma- 
tions, instead  of  perishing  within  twenty- four  hours  with  sep- 
ticemia as  they  would  if  they  had  not  been  protected  against 
this  organism.  In  chronic  cases  of  swine  plague,  as  found  in 
certain  outbreaks,  the  bacteria  are  often  attenuated  so  that 
when  inoculated  into  susceptible  rabbits  the  result  is  the  same 
as  when  the  rabbits  protected  by  partial  immunization  were 
inoculated  with  virulent  cultures.  The  above  simple  formula 
which  was  worked  out  and  demonstrated  for  certain  swine 
diseases  seems  to  apply  to  infectious  diseases  generally. 

§  g.  Classification  or  grouping  of  the  infectious  dis- 
eases. It  will  be  found  in  the  study  of  the  morbid  anatomy 
of  the  various  specific  maladies  that  the  lesions  in  a  given  dis- 
ease vary  in  different  species  and  in  individuals  of  the  same 
species  to  a  marked  degree.  This  fact  precludes  the  possibility 
of  classifying  or  arranging  them  after  their  morbid  anatomy,  if 
the  idea  of  a  specific  etiology  is  to  be  adhered  to.  If  the  infec- 
tious diseases  are  to  be  considered  as  parasitisms,  as  they 
appear  to  be,  the  only  logical  method  of  classifying  them, 
according  to  the  writer's  opinion,  is  the  one  suggested  by  their 
etiology,  namely,  that  they  shall  be  placed  in  groups  corre- 
sponding to  their  causes.  Thus  a  single  lesion  found  in  the 
glands  of  the  head,  in  the  lungs,  in  the  liver,  in  the  mesenteric 


CAUSE    FOR    VAKIATION 


17 


Fig.  4.  Large  abscess  in  partially  immunized  rabbit  caused  by  sivine- 
plague  bacteria.  This  rabbit  lived  37 1  days  after  its  inoculation  with 
virulent  swine  plague  bacteria.  At  death  its  -weight  zvas  19S0  grams\ 
the  tumor  itself  iveighing  goo  grams.  'J he  abscess  Jormed  dorsad  0/ the 
peritoneum.  [a)  Cecum,  [b]  intestines,  (c)  abscess.  The  control  rab- 
bit of  same  iveight  and  age  died  of  septicemia  in  16  hours. 


l8  CLASSIFICATION    OF    DISEASES 

glands,  in  the  skin,  in  the  joints,  or  in  the  generative  organs, 
would  be  called  tubercular  if  the  bacteria  of  tuberculosis  could 
be  demonstrated  to  be  its  cause.  The  same  conclusion  would 
be  maintained  regardless  of  the  character  of  the  lesion, 
whether  cellular,  purulent,  caseous  or  calcareous.  These  facts 
are  enough  to  suggest  that  the  most  direct  method  of  arrang- 
ing these  diseases  for  purposes  of  study  is  in  groups  composed 
of  like  generic  etiological  factors. 

Most  of  the  known  specific  causes  of  the  infectious  dis- 
eases of  animals  are  bacteria.  It  is  necessary,  therefore,  in 
carrying  out  this  plan  to  choose  from  among  the  numerous 
classifications  one  to  be  followed  in  grouping  the  diseases  ac- 
cording to  the  genera  of  bacteria  producing  them.  Of  the 
various  systems,  the  one  by  Migula  seems  to  be  the  simplest 
and  most  natural  and  consequently  it  is  selected.  The  only 
radical  difference  between  it  and  the  others,  so  far  as  pathol- 
ogy is  concerned,  rests  in  the  fact  that  the  old  genus  Bnderiu?n 
is  revived,  but  with  a  new  meaning.  All  rod-shaped,  non- 
motile  bacteria  are  placed  in  this  genus.  This  causes  a  change 
of  the  generic  name  from  Bacillus  to  Bacterium  of  a  number  of 
pathogenic  bacteria,  such  as  those  of  tuberculosis,  anthrax, 
swine  plague  and  others  of  less  importance. 

Because  of  the  few  species  of  fungi  and  protozoa  that 
are  pathogenic  for  animals,  systematic  classifications  of  these 
organisms  are  not  introduced.  For  such  classifications  the 
student  is  referred  to  the  various  works^ou  mycology  for  the 
fungi  and  the  excellent  work  by  Calkins,  — "  The  Protozoa" 
for  the  protozoa.  In  this  elementary  pathology,  all  that  seems 
to  be  necessary  concerning  the  biology  and  classification  of  the 
pathogenic  protozoa  will  be  given  in  connection  with  genera 
and  species  under  the  "  etiology  ' '  of  the  diseases  they  produce. 

The  chapter  on  diseases  caused  by  fungi  naturally  fol- 
lows those  on  the  bacterial  diseases. 

§  ID.  Migula's  classification  of  bacteria.  The  genera 
of  the  five  families  are  incladed. 


migula's  classification  of  bacteria  19 

MIGULA'S    CLASSIDCATION 

LOWER  BACTERIA 


COCCACCAC 


Streptococcus 

Mtcrococcus 

Sarcma 

Planococcus 

Planosarcma 

Bacterium 

Bacillus 

Pseudomonas 

Spirosoma 
Mlcrospira 
Spirillum 
Spirochaeta 


,»»u 


•  ••••     00   0000 


••  5^  @.*.  A-jJiflgj 


urn 


BACTERIACEAE 


#(^      7f    ^ 


SPIRILLACEAE 


MIGULA  S    CLASSIFICATION   OF    BACTERIA 


FAMILIES. 

I.  Cells  globose  in  a  free  state, 
not  elongating  in  any  direc- 
tion before  division  into  1,2, 
or  3  planes i. 

II.  Cells  cylindrical,  longer  or 
shorter,  and  only  dividing  in 
I  plane,  and  elongating  to 
twice  the  normal  length  be- 
fore the  division. 

(i)  Cells  straight,  rod-shaped, 
without  sheath,  non-motile, 
or  motile  by  means  of  fla- 
gella 2. 

(2)  Cells  crooked  without  sheath  3. 

(3)  Cells  enclosed  in  a  sheath 4. 

(4)  Cells   destitute   of   a   sheath, 

united  into  threads,  motile 
by  means  of  an  undulating 
membrane 5. 


Coccaceae. 


Bacteriacese. 
Spirillaceae. 
Chlamydobacteriaceae. 


Beggiatoaceae. 


I .      Coccacete. 


Cells  without  organs  of  motion. 

a.  Division  in    i    plane i. 

b.  Division  in  2  planes 2. 

c.  Division  in  3   planes 3. 

Cells  with  organs  of  motion. 

a.  Division  in  2  planes 4. 

b.  Division  in  3  planes 5. 

2.     Badcriaccie. 

Cells  without  organs   of  motion,    i. 
Cells   with     organs      of    motion 

(flagella). 


Streptococcus. 

Micrococcus. 

Sarcina. 

Planococcus. 
Planosarcina. 


Bacterium. 


migula's  classification  of  bacteria 

a.     Flagella  distributed  over 

the  whole  body 2.     Bacillus. 

d.     Flagella  polar 3.     Pseudomonas. 

3.      Spirillacece . 

Cells  rigid,  not  snakelike  or  flex- 
uous. 

a.  Cells  without  organs   of 

motion i.     Spirosoma. 

b.  Cells  with  organs  of  mo- 
tion (flagella). 

1.  Cells  with  one,  very 
rarely  2-3  polar  fla- 
gella    2.      Microspira. 

2.  Cells  of  polar  flagella, 

in  tufts  of  from  5-20- -   3.     Spirillum. 

Cells  flexuous 4-     Spirocha^ta. 


4- 


ChhxDiydobactcriaceae. 


Cell    contents    without    granules 
of  sulphur. 
A.      Cell  threads  unbranched. 

1 .  Cell  division  always  only 

in  I  plane i.     Streptothrix. 

2.  Cell  division  in  3  planes 
previous  to  the  forma- 
tion of  conidia. 

a.  Cells  surrounded  by  a 
very  delicate,  scarce- 
ly    visible     sheath 

(marine) 2.     Pliragnudiothrix. 

b.  Sheath  clearly  visible 

(in  fresh  water) 3.     Cretwi/trix. 


22  miguIvA's  classification  of  bacteria 

B.     Cell     threads     branched 

(pseudo- branches) 4.      Cladothrix. 

Cell    contents     containing     sul- 
phur granules 5.      Thiothrix. 

5.     Beggiatoaceae. 

Only  one  genus  known  {Beggiatoa  Trev.),  which  is 
scarcely  separable  from  Oscillaria.  Character  as  given  under 
the  family. 

REFERENCES. 

1.  Berger.  Vergleichende  Untersuchungen  iiber  den  Bacillus 
pyogenes  bovis  und  den  Bacillus  pyogenes  suis.  Zeitsch  f.  Iiifektiou- 
skrankh.  parasitare  k'raiikh.  und  Hygiene  der  Haustiere,  Bd.  Ill 
(1907),  S.   loi. 

2.  Grips.  Ueber  eine  mit  multipler  Abszessbildung  verlaufende 
Pleuritis  und  Peritonitis  der  Schweine  und  deren  Erreger.  Zeitschr.  f. 
Fleisch-  u.  Milchhygiene,  iSgS. 

3.  Grips.  Ueber  einen  pyogenen  Mikroorganismus  des 
Schweines.     Inaugural-Dissertation.     Giessen,  1902. 

4.  KiJNNEMANN.  Ein  Beitrag  zur  Kenntnis  der  Eitererreger  des 
Rindes.     Arch.  f.  zviss.   u.  prakt.     Tierheilk.,  1903. 

5.  MiGULA.     System  der  Bacterien.     1897. 

6.  vSmith  and  Moore.  On  the  variability  of  the  infectious  dis. 
eases  as  illustrated  by  hog  cholera  and  swine  plague.  Bulletin  No.  6. 
U.  S.  Bureau  of  Animal  Industry,   1894.     p.  81. 

7.  Welch.  General  bacteriology  of  surgical  infections.  Dennis^ 
System  of  Surgery.     Vol.  i ,  p.  249. 


CHAPTER    II. 


DISEASES    ATTRIBUTED    TO    WOUND    INFECTION. 


§  II.  Lesions  which  may  be  caused  by  several 
organisms  that  are  recognized  as  distinct  maladies.  It 
has  already  been  stated  that  the  lesions  following  wound 
infections  may  be  brought  about  by  a  variety  of  bacteria  and 
also  that  certain  of  these  disease  processes  are  sometimes 
recognized  as  distinct  maladies.  There  are  a  number  of  affec- 
tions which  belong  to  this  class.  From  some  of  these,  such  as 
botryomycosis,  a  supposedly  specific  organism  has  been  isolated 
and  described.  A  number  of  workers,  however,  have  found 
that  other  bacteria  may  produce  apparently  the  same  morbid 
conditions.  The  more  important  of  the  affections  which  seem 
to  be  directly  traceable  to  wound  infection  will  be  briefly  de- 
scribed in  the  light  of  recent  investigations.  It  should  be 
stated,  however,  that  the  amount  of  work  that  has  been  done 
on  these  subjects  is  not  sufficient  to  preclude  the  possibility  of 
a  specific  etiological  factor,  but  rather  to  suggest  the  lines 
along  which  valuable  and  more  conclusive  findings  may  be 
expected  in  the  future. 


§  12.  Botryomycosis,  This  name  has  been  given  to  a 
variety  of  lesions  found  more  commonly  in  the  horse  but  oc- 
curring also  in  cattle,  swine  and  other  animals.  The  thickened 
spermatic  cord  (scirrhous  cord)  which  sometimes  follows  cas- 
tration is  the  most  common  form  of  this  disease.  Practitioners 
often  designate  as  botryomycosis  certain  closed  abcesses  occur- 
ring in  the  subcutaneous  or  intermuscular  tissue.  Abscesses 
and  nodules  found  in  the  internal  organs  have  been  included 
under  this  caption.     Several   investigators  have  isolated  from 


24  BOTRYOMVCOSIS 

these  lesions  a  species  of  microorganism  which  appeared  to 
stand  in  a  causative  relation  to  them.  It  was  first  described  as 
Zobgloea  pulmonis  equi,  in  1870,  b}^  Bollinger  who  found  it  in 
the  nodules  in  the  lungs  of  a  horse.  More  recently  he  re- 
named it  Botryococcus  ascoformans.  Rivolta  designated  it  Dis- 
comyces  equi.  Rabe  proposed  the  name  Mkrococais  botryogenes 
and  Johne  has  called  it  M.  ascoformans.  The  results  of  other 
investigations  throw  some  doubt  upon  the  specific  nature  of 
these  lesions.  Kitt,  Hell,  dejong,  Gay  and  others  have  found 
in  them  micrococci  which  do  not  differ  from  M.  pyogenes  aureus. 
The  writer  has  failed  to  find  M.  ascoformans  but  has  isolated 
in  its  stead  pyogenic  micrococci  and  streptococci.  In  one  very 
interesting  case  of  thickened  cord,  the  writer  found  masses  of  a 
fungus  resembling  that  of  actinomycosis  within  the  pockets  of 
spongy  tis.sue  sprinkled  throughout  the  thickened  fibrous  cord. 
Bacteria  was  not  found  in  this  case. 

In  the  closed  abcesses  in  the  connective  tissue,  pyogenic 
bacteria  have  been  found,  excepting  in  certain  cases  of  long 
standing  where  the  cultures  give  negative  results.  Investi- 
gations which  have  been  made  into  the  bacterial  flora  of  the 
skin  of  the  horse  show  that  pyogenic  bacteria  are  frequently 
present  in  the  deeper  layers  of  the  epidermis,  in  ducts  of  glands 
and  about  the  hair  shafts.  With  the  possibility  of  infection 
from  the  integument  plus  all  the  other  chances  of  having 
members  of  this  and  other  groups  of  bacteria  introduced  into 
the  body  there  seems  to  be  abundant  opportunity  for  infection 
wnth  a  variety  of  species.  The  evidence  at  hand  points  to  the 
conclusion  that  botryomycosis  is  the  result  of  wound  infection, 
and  that  several  species  of  microorganisms  are  capable  of  pro- 
ducing it,  especially  the  form  known  as  scirrhous  cord. 

The  source  of  infection  in  the  cord  is  to  be  found  in  the 
unsterilized  or  non- disinfected  skin,  improperly  sterilized  in- 
struments, dressings,  and  hands  of  operator.  For  precautions 
to  be  observed  in  disinfecting  the  skin  see  chapter  on  disinfec- 
tion. The  fact  is  worthy  of  note  in  this  connection,  that  sep- 
ticemia, peritonitis,  and  other  more  distantly  localized  lesions 
occasionallv  follow  such  infections. 


OMPHALOPHLKBITIS 


^13.  Omphalophlebitis.  This  affection  which  is  com- 
monly called  navel- ill,  consists  of  suppurative  lesions  in  young 
animals  caused  by  pyogenic  bacteria.  In  the  horse  they  are 
most  often  localized  in  the  joints  of  the  limbs.  In  certain  other 
species  the  lesions  are  quite  as  likely  to  be  situated  elsewhere 
in  the  body.  In  some  cases  the  morbid  changes  are  restricted 
to  subcutaneous  and  intermuscular  suppurative  cellulitis. 

The  infection  takes  place  in  the  umbilicus.  As  the  cord 
is  severed  in  the  field  or  stable  many  species  of  bacteria  may 
gain  access  to  the  end  of  the  exposed  and  freshly  severed  cord. 
In  the  colt  a  streptococcous  seems  to  be  the  most  common 
species  of  bacteria  capable  of  producing  the  joint  abscesses. 
In  the  lamb,  a  variety  of  the  colon  bacillus  has  been  associated, 
apparently  as  the  etiological  factor,  with  the  subcutaneous 
cellulitis.  The  lesions  resulting  from  navel  infection  illustrate 
in  a  most  excellent  manner  the  extent  to  which  certain  pyo- 
genic bacteria  gaining  access  to  the  body  may  extend  by 
metastasis  to  places  remote  from  their  entrance  and  produce 
diseased  foci. 

In  the  case  of  navel-ill.  the  umbilical  vein  contains  a  large 
number  of  bacteria.  The  writer  has  found  that  in  colts  very 
few  if  any  of  the  bacteria  (streptococci)  producing  the  joint 
lesions  could  be  found  in  the  parenchymatous  organs.  Occas- 
sionallv  one  or  two  of  many  tubes  of  media  inoculated  from 
the  liver  would  develop  into  cultures  of  the  infecting  organism. 
In  this  disease,  where  many  species  of  bacteria  come  into  com- 
petition, one  is  impressed  with  the  fact  that  seemingly  very 
few  of  the  ordinary  bacteria  are  capable  of  gaining  an  entrance 
into  the  circulation  or,  at  least,  are  possessed  of  vital  powers 
sufficient  to  resist  the  destructive  forces  of  the  living  animal 
body  A  brief  description  of  a  case  with  the  bacterial  findings 
win  illustrate  this  point.  The  case  referred  to  was  from  Dr. 
Williams'  clinic. 

A  colt,  about  three  years  old.     It  was  in  good  condition  ^^^^^^^^^'f 
to  be  perfectly  well  excepting  for  the  diseased  joints.     It  was  killed  tor 


26  WHITE    SCOURS    IN    CALVES 

examination.  The  umbilical  vein,  from  the  umbilicus  to  the  liver,  was 
distended  with  blood,  pus  cells  and  bacteria.  All  the  internal  organs 
appeared  to  be  normal.  In  both  knee  joints,  and  in  one  hock  joint  there 
was  extensive  suppuration.  A  bacteriological  examination  showed  the 
umbilical  vein  to  contain  many  species  of  bacteria,  among  which  may  be 
mentioned  B.  coli  coniinunis^  Micrococcus  pyogenes  aureus  and  a  strep- 
tococcus. One  of  several  tubes  of  media  inoculated  from  the  liver  de- 
veloped the  streptococcus,  the  others  remained  clear.  All  media  inocu- 
lated from  the  heart  blood,  spleen,  kidney  and  glands  remained  sterile. 
All  of  the  media  inoculated  with  the  pus  from  the  diseased  joints  gave 
pure  cultures  of  the  streptococcus. 

The  treatment  in  these  cases  is  limited  to  the  prevention. 
The  proper  disinfection  and  dressing  of  the  umbiHcus  at  the 
time  it  is  severed  prevent  this  trouble.  It  is  the  only  pre- 
ventative measure  known  to  us. 


§  14.  W^hite  scours  or  diarrhea  in  calves.  This  is 
a  disease  affecting  calves  from  a  few  hours  to  as  many  days 
old,  with  a  mortality  ranging  from  50  to  90  per  cent.  The  in- 
vestigations which  have  been  made  in  this  country,  especially 
those  at  the  New  York  State  Veterinary  College,  have  sug- 
gested that  it  is  due  to  certain  forms  of  the  colon  bacillus.  In 
these  investigations  characteristic  lesions  were  not  found. 

Nocard  reported  the  results  of  his  investigation  of  appar- 
ently a  similar  disease  of  calves  in  Ireland.  He  found  that 
they  usually  die  during  the  first  week.  In  the  more  chronic 
cases,  lung  lesions  were  found.  His  inquiries  tend  to  show 
that  this  is  primarily  due  to  a  wound  infection.  He  states  in 
his  report  concerning  the  nature  of  this  disease  that  it  usually 
lasts  from  3  to  6  days  and  is  characterized  by  an  intense  intes- 
tinal discharge.  The  discharges  are  always  of  the  nature  of  a 
diarrhea,  white  and  frothy.  The  calves  lose  flesh  rapidly, 
their  flanks  are  hollow,  abdomen  retracted,  back  arched,  eyes 
sunken,  and  hair  dull  ;  they  make  violent  expulsive  efforts, 
the  nose  is  hot  and  dry  with  slight  discharge  of  mucus,  and 
the  temperature  is  elevated. 

In  other  cases,  but  not  so  commonly,   the    symptoms  are 


WHITE    SCOURS    IN    CALVKS 


27 


less  severe  and  recovery  seems  to  take  place  ;  but  most  of  the 
calves  die  several  weeks  later  with  pulmonary  lesions. 

Nocard  states  that  it  is  not  rare  to  see,  in  these  cases, 
the  discharges  mixed  with  blood  in  various  quantities.  In 
more  chronic  forms  it  is  not  rare  to  observe  acute,  multiple  and 
very  painful  arthritis. 

The  lesions  found  at  the  autopsy  vary  according  to  the 
course  of  the  disease.  Usually  the  umbilicus  is  large  and  the 
umbilical  blood  vessels  have  indurated  walls,  and  contain 
blood  clots  which  may  be  soft  and  purulent.  Bloody  extrav- 
asations are  observed,  sometimes  ver\'  extensive,  along  the 
umbilical  vessels  and  the  urachus,  extending  sometimes  to 
the  posterior  third  of  the  bladder. 

In  rapidly  progressing  cases,  lesions  of  true  hemorrhagic 
septicemia  are  found.  All  the  organs  are  congested  ;  their 
surface  is  covered  with  petechiae,  ecchymoses  or  sub-serous 
blood  infiltrations  ;  the  capillary  network  of  the  peritoneum, 
the  omentum,  the  pleura  and  the  pericardium  is  very  much 
injected. 

Nocard  describes  the  lungs  and  articular  lesions  as  follows  : 

"The  lungs  are  rarely  entirely  healthy  ;  most  often  they 
present  here  and  there  little  diffuse  centers  of  catarrhal  pneu- 
monia, nodular  broncho-pneumonia  or  only  of  atelectasis.  The 
lesions  are  much  more  constant,  extensive  and  dense  when  the 
animals  have  resisted  longer  ;  they  represent  then  the  transi- 
tion between  the  simple  atelectasis  of  the  beginning  and  the 
suppurative  lesion  of  lung  disease. 

"Articular  lesions,  when  they  exist,  are  very  interesting. 
The  periarticular  tissues  are  infiltrated  with  yellowish  and 
somewhat  gelatinous  liquid  ;  the  synovial  serous  membrane  is 
covered  with  a  rich  vascular  injection,  which  seems  to  extend 
to  the  borders  of  the  cartilages  of  the  articular  surfaces  ;  the 
culs-de-sac  of  the  synovials  are  distended  by  a  great  quantity 
of  thick  and  limpid  synovia,  strongly  yellow  or  reddish  in 
color,  and  in  which  more  or  less  dense  and  abundant  clots  ot 
fibrinous  exudate  are  floating.  When  the  lesion  is  older, 
instead  of  synovia,  there  are  thick,  dense,    and    firm   fibrinous 


28  WHITE    SCOURS    IN    CALVES 

exudates,  which  fill  the  culs-de-sac  of  the  serous  membrane 
and  are  infiltrated  between  the  articular  surfaces.  In  these 
cases  the  lesion  resembles  exactly  those  of  peripneumonic 
arthritis  of  sucking  calves." 

He  found  a  microorganism  (Pasteurella)  in  the  organs 
and  blood  of  the  calves,  with  which  he  was  able  to  produce 
the  disease.  After  convincing  himself  that  he  had  found  the 
cause,  he  sought  for  the  source  of  infection,  which  he  found 
in  the  umbiliais.  He  advances  three  suppositions  concerning 
the  time  and  mode  of  entrance  :  i.  intra-uterine,  2.  vaginal, 
3.  after  delivery  when  the  calf  drops  on  the  ground  or  floor 
and  when  the  ruptured  cord  conies  in  contact  with  the  fecal 
matter  or  dust  of  the  stable.  The  latter  he  believes  to  be  the 
actual  method.  His  conclusion  concerning  infection  after 
delivery  may  be  summarized  in  the  following  observation 
which  he  makes  : 

"  We  have  witnessed  in  a  well  kept  farm  a  case  of  labor 
in  a  cow.  She  was  in  an  ordinary  barn.  Nothing  had  been 
prepared  to  receive  the  new-born.  The  calf  was  dropped  on  a 
bedding  soiled  with  feces  ;  he  only  fell  back  a  little,  and  there 
during  15  or  20  minutes,  we  watched  him  making  his  efforts 
to  get  up,  falling  back  here  and  there  to  the  right  and  to  the 
left  or  on  his  belly,  dragging  the  stump  of  his  cord  on  the 
ground,  in  the  urine,  or  even  in  the  fecal  matter.  It  was  only 
after  the  mother  had  well  licked  her  little  one,  well  covered 
with  salt,  that  the  cord  was  ligated.  I  am  not  sure  that  the 
umbilicus  was  cleaned. 

"  White  scours  is  ordinarily  the  result  of  iDnbilical  infection 
which  takes  place  at  the  time  of  delivery,  by  the  way  of  the 
wound  made  by  the  rupture  of  the  cord." 

He  states  that  this  trouble  can  be  prevented  if  the  person 
in  charge  of  the  animals  at  the  time  of  their  delivery  takes 
certain  precautious  to  prevent  infection. 

This  disease  described  by  Nocard  does  not  seem  to  differ 
in  many  respects  from  the  diarrhea  in  young  calves  in  this 
country.  Lesage  and  Delmar  have  described  the  disease  in 
France.     Ward  and  Fisher  tested  Nocard's  method  with  quite 


SUPPURATIVE    CELLULITIS  29 

satisfactory  results  In  our  cases  the  lung  complications  did 
not  occur  Our  bacteriological  examination  of  a  number  of 
young  calves  that  died  of  this  trouble  showed  that  their  blood 
and  organs  were  teeming  with  a  variety  of  B.  coU  communis. 
I  have  not  found  Bad.  sept,  hemorrhagicce  (Pasteurella)  in 
any  of  our  cases.  This  suggests  the  possibility  of  serious 
umbilical  infection  with  members  of  other  groups  of  bacteria. 
The  important  finding  of  Nocard  should  stimulate  further  in- 
vestigation into  this  important  trouble  in  this  country.  As 
the  remedy  which  he  recommends,  and  which  has  given  good 
results  is  simplv  one  to  prevent  infection  of  the  ruptured  cord, 
the  conclusion  of  the  wound  infection  origin  of  this  disease  is 
strengthened. 


^  15.  Infectious  suppurative  cellulitis.  Cattle  and 
sheep  suffer  from  more  or  less  extensive  inflammatory  condi- 
tions of  the  subcutaneous  tissues,  especially  of  the  lower 
extremities.  Frequently  the  morbid  process  extends  beneath 
the  hoof,  causing  it  to  slough  or  to  undergo  resulting  disinte- 
gration changes.  When  this  condition  exists,  the  affection  is 
usually  called  "foot  rot."  If  the  inflammatory  process  attacks 
the  skin  also,  the  condition  is  often  designated  erysipelas.  If 
it  becomes  circumscribed,  resulting  in  a  local  suppuration  an 
abscess  or  an  ulcer  is  the  result.  The  investigations  which 
have  been  made  concerning  the  cause  of  these  lesions  point  to 
the  conclusion  that  they  result  from  an  infection,  probably 
through  some  slight  abrasion  of  the  skin.  Thus  far.  the 
results  show  .streptococci*  to  be  the  etiological  factors  m  the 
majority  of  these  cases.  It  frequently  happens  that  a  number 
of  animals  subjected  to  the  same  conditions  are  attacked  at  the 
same  time,  giving  rise  to  a  condition  resembling   an  epizootic. 

*Lu^et^s  reported   the  results  of  bacteriologic  examinations    of 
fifty-two   abscesses   in  cattle.     From  nine  of    these    steptococci    were 
obtained  in  pure  culture,  and  in   ten   cases   ^^ey  were   -    -t-^^  ^ 
other  bacteria.-^;/;/^/^.-  de  V  Instilut  Pasteur.     Vol.  I  II(iS^3),P-  .-^f- 


30  SUPPURATIVE    CELLULITIS 

In  cattle, — cases  studied  by  the  writer, — the  lesions  were, 
within  certain  limits,  uniform  in  all  of  the  affected  animals. 
Usually  but  one  foot  or  leg  was  attacked,  although  there  were 
numerous  exceptions.  The  first  symptom  noticed  was  a  swell- 
ing, which  usually  appeared  in  the  lower  part  of  the  leg,  most 
often  in  the  pastern.  In  some  animals  the  swelling  was  re- 
stricted to  a  small  area,  but  often  it  extended  up  the  leg  to 
and  even  above  the  knee  or  hock  joint.  There  was  evidence 
of  pain.  As  the  inflammator}' process  continued,  the  subcutane- 
ous tissue  became  indurated,  the  skin  thick  and  dry,  and  later 
it  would  crack,  usually  but  not  always,  below  the  dew  claws, 
and  a  thick  creamy  pus  would  be  discharged.  After  discharg- 
ing, the  swelling  subsided  and  the  normal  condition  was 
rapidly  restored.  The  time  necessary  for  the  suppurative 
process  and  recovery  to  take  place  varied  in  different  animals, 
but  as  a  rule  from  ten  to  fifteen  days  were  required.  The 
exceptions  were  largely  in  those  cases  where  the  inflammatory 
process  extended  down  to  the  coronary  cushion.  In  these 
there  was  more  or  less  sloughing  of  the  hoof.  These  cases 
were  the  most  serious. 

In  the  so-called  foot-rot  of  sheep,  we  have,  in  the  cases 
which  have  come  to  our  notice,  conditions  similar  to  those 
found  in  the  cattle  which  were  suffering  from  suppurative  cellu- 
litis. It  may  be  of  interest  to  cite  a  specific  case  with  the 
result  of  the  bacteriological  examinations. 

May,  1899,  two  sheep  that  were  suffering  from  so-called 
foot-rot  were  brought  to  Dr.  Law's  clinic.  They  came  from  a 
large  flock  in  which  forty  or  more  animals  were  reported  to  be 
similarly  affected. 

No.  I.  An  adult  female  in  very  poor  condition.  All  four  feet  and 
legs  were  affected  and  the  nails  on  one  foot  were  quite  loose.  There 
was  a  purulent  discharge  from  openings  either  between  the  claws  or  in 
the  skin  just  above  the  hoof.  The  microscopic  examination  of  the  pus 
from  this  opening  showed  a  number  of  bacteria,  but  streptococci  were 
especially  numerous.  They  were  not  isolated  in  pure  culture.  The 
left  knee  was  badly  swollen  and  from  the  lower  side  of  the  swelling 
there  was  a  discharge  of  thin  purulent  substance  which  contained  strep- 


FisTULOiT.s  \vithp:r.s  3! 

tococci  in  large  numbers.     A  few  other    bacteria,    mostl)"    micrococci, 
were  associated  with  them. 

No.  2.  An  adult  female,  black,  emaciated,  but  in  much  better  flesh 
than  No.  i.  The  two  fore  feet  and  the  left  hind  one  were  affected.  The 
hind  foot  and  the  right  fore  one  were  discharging.  The  left  fore  foot 
was  badly  swollen  above  the  hoof  but  the  swelling  did  not  extend  high 
up  the  leg.  Fluctuation  was  marked.  The  skin  was  shaved,  washed, 
disinfected  and  the  abscess  opened.  A  thick  creamy  pus  was  expressed. 
From  this  a  number  of  tubes  of  media  were  inoculated  and  in  each  a 
streptococcus  developed  in  pure  culture.  The  pus  from  the  discharging 
feet  contained  a  streptococcus  with  other  bacteria.  The  feet  were 
treated  locally  with  disinfectants  by  Dr.  Law.  In  recovering  there  was 
considerable  thickening  of  the  interdigital  tissue.  In  this  case  the 
suppuration  had  not  extended  under  the  nails. 


§  16.  Fistulous  withers  and  poll-evil.  Recent  inves- 
tigations indicate  that  these  very  common  and  troublesome 
local  diseased  conditions  are  either  directly  or  indirectly  the 
result  of  bacterial  invasion.  This  conclusion  is  tentatively 
drawn  from  the  fact  that  the  bacteriological  examinations  made 
from  the  pus  and  from  recent  lesions  in  these  affections  invari- 
ably reveal  the  presence  of  streptococci  or  micrococci,  or  both. 
Gaj'  found  a  streptococcus  in  each  of  seven  cases  of  common 
fistulous  withers  and  in  two  cases  of  poll-evil.  It  was  invari- 
ably a.ssociated  with  a  micrococcus.  He  found  in  five  cases  of 
deep  seated  shoulder  abscesses  M.  pyogenes  aureus  only.  It  is 
instructive  to  note,  that  bacteria  closely  resembling  this  organ- 
ism have  frequently  been  found  in  the  deeper  layers  of  the  skin. 
The  mechanical  injuries  commonly  attributed  as  the  primary 
cause  consist  usually  of  little  more  than  skin  irritation  from  ill 
fitting  harnesses,  saddles  or  from  blows.  While  these  are 
mechanically  not  extensive,  they  are  sufficient  to  liberate  into 
the  juices  of  the  subjacent  tissues  the  bacteria  deeply  seated  in 
the  integument.  The  inflammatory  process  leading  to  sup- 
puration, the  formation  of  fistul^e,  the  new  formation  of  fibrous 
tissue  in  the  affected  parts,  and  even  the  bone  necrosis  occa- 
sionally seen  are  all  possible  and  rational  results  of  the  activi- 
ties of  the  pyogenic  bacteria  found  in    the    lesions.     There   is 


32 


INFECTIOUS     MASTITIS 


nothing  in  their  character  to  suggest  causative  agencies  other 
than  microorganisms.  The  tissue  changes  involved  in  the 
deposition  of  fibrous  tissue  and  the  abscess  formation  are 
known  as  the  results  of  infection  and  the  inflammatory  pro- 
cesses following  them.  These  affections  are  mentioned  in  this 
connection  simply  because  the  accumulating  evidence  tends  to 
strengthen  the  working  hypothesis  that  they  are  the  result  of 
bacterial  invasion. 


Cattle  suffer  frequently  from 
an  acute  inflammation  of  the  udder  as  the  result  apparently  of 
an  invasion  by  a  number  of  bacteria.     The  results  of  the  inves- 
tigation   of  this  affection  thus  far  reported  suggest  that  the 
form  which  is  transmitted  from  animal  to  animal  is  caused  by 
a  streptococcus.     It  is,  however, 
difficult   to  distinguish    between 
this  affection  and  those   caused 
by    certain    other    bacteria.       It 
t      "••••'  -j»  ^  \  t         seems  likely  that  many  cases  are 

\    /^  i  •    *  ,•••••••*  primarily  brought  about  by  me- 

•  '''''^.      *To     ••••••**>*      •  chanical    injuries   which    render 

possible    the    entrance    into   the 
fresh  tissues  of  the  bacteria  of  the 
skin  or  of  the  milk  ducts.     Other 
cases  may    be    due    to    infection 
through  the  teat  of  bacteria  capa- 
FiG.  5.      Streptococcics  from  a    ^^j^  ^f  producing,   by    means  of 
case  of  infectious   mastitis.  ,     .  ...  j      ^      ^-l      • 

their  metabolic  products,  the  in- 
flammatory condition  without  a  distinct  injury  to  the  mucous 
membrane.  The  former  view  that  there  was  a  sphincter  mus- 
cle near  the  base  of  the  teat  which  closed  the  duct  sufficiently 
to  prevent  the  entrance  of  bacteria  to  the  secreting  portions  of 
the  gland  was  not  well  founded  upon  anatomical  facts  (Fig.  6). 
The  acute  and  more  chronic  inflammatory  affections  of  the 
udder  fall  very  naturally  into  two  groups,  namely  :  (i)  those 
in  which  the  parenchyma  is  most    affected    and    (2)    those  in 


INFECTIOITS    MASTITIS 


33 


which  the  stroma  or  fibrous  tissue  is  involved.  The  form  of 
mastitis  more  frequently  encountered  as  an  infectious  (trans- 
missible) disease  is  characterized  by  very  marked  changes  in 
the  milk,  accompanied  by  the  usual  symptoms  of  parenchymat- 
ous inflammation  of  the  gland  itself.  The  discharge  from  the 
udder  usually  contains  flaky  masses  held  in  suspension  in  the 
clear  or  perhaps  cloudy  serum.  The  color  varies,  and  occa- 
sionally the  fluid  is  blood-stained.  The  microscopic  examina- 
tion shows  the  presence  of  agglutinated  fat  globules,  pus  cells 
and  often  red  blood  corpuscles. 

A  number  of  bacteria*  considered  of  more  or  less  etiologi- 
cal value  have  been  found  associated  with  lesions  of  doubtful 
specific  origin.  The  results  of  Kitt,  Nocard,  Mollereau,  Guille- 
beau,  Zschokke,  Bang  and  still  others,  in  which  a  Bacterium, 
a  Bacillus,  a  Micrococcus ,  a  Staphylococcus,  and  a  Streptococcus 
have  been  found  and  reported  as  standing  in  a  causal  relation 
to  the  trouble,  indicate  that  a  variety  of  microorganisms  are 
active  in  producing  those  affections  which  are  frequently 
grouped  without  distinction  as  infectious  mastitis.  The  review 
of  much  of  the  literature  on  this  subject  shows  that  a  number 
of  cases  reported  as  infectious  were  isolated  or  sporadic  ones, 
/.  e. ,  they  were  in  dairies  where  the  disease  did  not  spread  to 
other  animals.  While  these  may  be  truly  infectious  in  their 
nature  they  should  be  differentiated  from  the  rapidly  spread- 
ing phlegmons  which  are  easily  recognized  as  infectious 
(^contagious). 

If  we  take  into  account  the  variety  of  anatomical  changes 
which  have  been  described  in  the  various  udder  affections,  we 
can  reasonably  admit  that  different  agencies  may  have  been 
instrumental  in  their  production.  The  various  species  of  bac- 
teria which  have  been  isolated  from  the  udder  lesions  may  very 


*Among  the  bacteria  which  have  been  found  in  udder  trouble  and 
described  as  a  possible  or  perhaps  the  more  probable  cause  the  follow- 
ing species  may  be  mentioned  :  Bacterium  phlegmasiic  uberis.  Strep- 
tococcus agalactitT  contagioscc,  Stapliylococcus  tnastitidis,  Galactococcus 
versicolor,  G.  fulvus,  G.  albus. 


34 


INFECTIOUS    MASTITIS 


^       ^ 


^"->^ 


Fig.  6.  Section  of  a  quarter  of  a  cow's  udder  through  one  teat; 
{a)  cistern,  (b)  larger  milk  ducts,  {0  secreting  portion  of  mammary 
gland.     2,  drawing  of  secreting  portion  of  gland,  enlarged. 


INFECTIOITS    MASTITIS  35 

likely  have  been  of  etiological  importance  in  their  respective 
cases. 

Already  the  facts  have  been  pointed  out,  that  the  udder  is 
normally  more  or  less  extensively  invaded  with  bacteria  and 
that  certain  species  of  bacteria  seem  to  persist  in  the  milk 
ducts  of  the  glands  when  once  they  become  lodged  there.  If 
these  results  apply  to  cows  generally  as  rigidly  as  they  did  to 
those  examined,  an  explanation  for  the  presence  of  a  variety 
of  bacteria  in  the  affected  udders  is  not  difficult  to  find. 
Whether  these  particular  organisms,  under  certain  conditions, 
would  become  primarily  responsible  for  udder  disease  is  not 
known.  The  evidence  suggests  that  a  number  of  the  bacteria, 
heretofore  described  as  the  cause  of  mammitis,  were  in  the 
affected  glands  by  virtue  of  their  presence  in  the  normal  udder. 
Concerning  these  points  additional  investigations  are  much 
needed. 

The  writer  has  examined  the  milk  secretions  from  the 
affected  cows  in  two  quite  serious  outbreaks  of  mastitis.  In 
the  first,  the  milk  was  drawn  in  sterile  bottles  after  the  udders 
and  the  hands  of  the  milker  had  been  thoroughly  washed  in  a 
I  to  I ooo  solution  of  corrosive  sublimate.  In  all,  there  were 
eight  samples  of  milk  taken  from  as  many  different  cows.  In 
six  of  the  eight  specimens  streptococci  appeared  in  pure  cul- 
ture. In  the  other  two  cases  micrococci  were  associated  with 
the  streptococcus.  In  the  second  outbreak,  the  milk  from  four 
diseased  udders  was  drawn  with  aseptic  precautions  directly 
into  tubes  containing  slant  agar  and  promptly  sent  to  the 
laboratory,  where  it  was  carefully  examined.  From  two  cases 
pure  cultures  of  streptococci  were  obtained,  while  those  from 
the  others  were  impure.  The  streptococci  obtained  from  the 
twelve  cases  appeared  to  be  identical  and  the  clinical  aspect  of 
the  disease  in  the  different  animals  w^as  the  same. 

In  a  dairy  that  was  under  close  observation  by  Ward,  one 
cow  was  found  to  be  troubled  in  one  quarter  of  the  udder  with 
an  inflammatory  process  which  produced  thickened  masses  in 
the  blood-stained  milk.  From  this  milk  a  streptococcus  was 
isolated  in  pure  culture.     It  could  not  be  diff-erentiated   from 


36 


MISCELLANEOUS    INFECTIONS 


the  one  isolated  from  the  cows  in  the  outbreaks  mentioned. 
Another  cow  in  this  herd  was  found  to  have  her  udder  per- 
manently infected  with  a  streptococcus.  Another  animal  in 
the  same  dairy  suffered  repeatedly  from  acute  streptococcus 
mastitis. 

There  are  a  large  number  of  morbid  conditions  more  or 
less  frequently  encountered  in  domesticated  animals,  which 
seem  to  be  due  to  infection  of  some  kind  but  which  are  not 
demonstrated  to  be  of  such  an  origin.  These  will  continue  to 
be  attributed  by  some  to  infection  and  by  others  to  various 
general  causes  until  the  truth  concerning  their  etiology  is 
revealed. 


j^  i8.  Miscellaneous  infections.  Attention  should  be 
called  to  the  many  morbid  conditions,  resulting  from  infection, 
that  are  encountered  in  different  species  of  animals  and 
are  liable  to  be  attributed  to  other  agencies.  Usually  such 
lesions  are  referred  to  general  pathological  conditions,  but  a 
more  careful  inquiry  will  reveal  the  presence  of  infection. 
Among  these,  may  be  mentioned  pericarditis  in  cattle,  so  fre- 
quently associated  with  punctures  by  foreign  bodies.  The 
extensive  exudative  inflammations  in  these  cases  are  frequently 
associated  with  micrococci.  The  same  has  been  true  of  certain 
cases  of  localized  endocarditis  resulting  in  the  formation  of  fun- 
goid, purulent,  or  necrotic  masses  about  the  valves  of  the  heart. 
When  one  considers  the  possibilities  of  infection  from  acci- 
dental causes,  as  well  as  from  surgical  interference,  together 
with  the  agency  of  metastasis,  it  is  not  difficult  to  understand 
how  such  a  variety  of  morbid  conditions  can  come  about. 
Infection,  therefore,  forms  an  important  part  of  pathology,  out- 
side of  those  specific  organisms  that  cause  epizootics  of  greater 
or  less  severity. 

REFERENCES. 

I.  Bollinger.  Mycosis  der  Lunge  beim  Pferd.  Archiv  fiir 
pathoL     AnaL,     Bd.  XUX  (1870),  S.  583. 


REFERENCES  37 

2.  DeJong.  Untersuchunt(en  iiber  Rotryoniyces.  These  de  Gies- 
sen,  1899. 

3.  Dubois.  An  enzooty  of  acute  streptococcic  mammitis.  /our. 
ofComp.  Pathology  and  Therapeutics,  Vol.  17  (1904),  p.  159. 

4.  Frohxkr.  Ein  Fall  von  generalisirter  Botryomykose.  Mouat- 
sheftefiir  Thierheilk.,     Bd.  VIII  (1897),  vS.  171. 

5.  (tAV.  a  bacteriological  study  of  fistulous  withers,  botryomy- 
cosis  and  infected  wounds  in  the  horse.  Ainer.  i^et.  Reviei<.\  Vol. 
XXIV  (i9oi),p.  877. 

6.  JOHNE.  Zur  Actinomykose  des  Sameustranges.  Deutsche  Zeit- 
schr.Jiir  Thierm.,     Bd.  XII  (1885 1,  S.  73. 

7.  LucET.     Ann.  de  P  Institut  Pasteur.     Vol.  VI  (1893)  p.  324. 

8.  M'Fadvicax.  Metastatic  lesions  in  Discomycosis.  The  Jour. 
Compr.  Path,  and  Thera.,  Vol.  XIII  (1900),  p.  337. 

9.  MiGULA.     System  der  Bacterien.     1897. 

ID.  Moore.  Suppurative  cellulitis  in  the  limbs  of  cattle  due  to 
streptococcus  infection.     Ainer.  Vet.  Reviezv,    June,  1898. 

11.  NocARD.  A  New  Pasteurellose  :  White  scours  and  lung  dis- 
ease of  calves  in  Ireland.  Anier.  Vet.  Reviezv.,  Vol.  XXV  (1901), 
p.  326. 

12.  Smith  and  Dawson.  Injuries  to  cattle  from  swallowing 
pointed  objects.  Ann.  Report  U.  S.  Bureau  of  Auitnal  Industry, 
1893-4,  p.  78. 

13.  W.-VRD.  The  invasion  of  the  udder  by  bacteria.  Bulletin  No. 
ijS,  Cornell  Univ.  Agric.  Exp.  Station,    1900. 


CHAPTER  III. 


DISEASES  CAUSED  BY  BACTERIA 
GENUS  STREPTOCOCCUS. 


§  19.  General  discussion  of  streptococci.  The  con- 
fusion which  exists  coucerning  species  in  this  group  of  bacteria 
and  the  variety  of  antistreptococcic  serums  on  the  market,  ren- 
der a  summary  of  the  present  knowledge  concerning  this  group 
of  bacteria  somewhat  desirable.  The  genus  Streptococcus  is 
based  according  to  Migula  on  its  method  of  reproduction  or 
division.  Streptococci  are  spherical  bacteria  that  divide  in  one 
plane.  The  segments  do  not  separate  but  are  held  together  in 
short  or  longer  chains,  although  the  divisions  seem  to  be  com- 
plete. Just  how  the  segments  are  held  together  is  not  fully 
determined.  According  to  older  and  more  commonly  encoun- 
tered classifications,  a  streptococcus  is  simply  a  number  of 
micrococci  (spherical  bacteria)  united  in  the  form  of  a  chain. 
In  some  of  the  supposedly  different  species  the  segments  are 
oblong  and  vary  in  size.  Frequently,  however,  the  segments 
vary  in  size  and  form  in  the  same  chain. 

The  more  usually  observed  cultural  characters  and  bio- 
chemic  properties  of  different  streptococci  are  quite  similar, 
although  it  is  difficult  to  obtain  two  cultures  that  will  exactly 
agree  in  all  of  their  manifestations  when  grown  on  a  large 
number  of  media.  Their  disease-producing  powers,  however, 
vary  within  wide  limits.  While  variations  in  the  physio- 
logical properties  and  pathogenesis  are  true  for  different  cul- 
tures (species?  ),  it  has  been  found  that  there  is  a  possibility  of 
much  variation  in  the  subcultures  of  the  same  species.  As 
with  certain  other  bacteria,  their  virulence  is  the  first  to  suffer 
change.  In  differentiating  species,  therefore,  the  fact  must 
not  be  overlooked,  that  the  existing  characters  and  properties 


STREPTOCOCCI  39 

possessed  by  the  streptoccocus  in  hand  may  have  been  more 
or  less  influenced  by  its  conditions  of  life.  When,  for  example, 
two  streptococci  appear  to  be  identical  under  the  majority  of 
tests,  a  slight  deviation  in  a  single  property  cannot  be  considered 
of  great  differential  value  especially  if  this  particular  manifes- 
tation is  among  those  most  subject  to  change.  A  fundamental 
difficulty  in  differentiating  species  among  streptococci  seems  to 
be  a  lack  of  information  concerning  the  possible  variations 
brought  about  by  different  environments.  The  further  diffi- 
culty of  identifying  any  of  the  very  large  number  of  forms 
which  have  been  assigned  specific  names  is  due  to  the  brevity 

•••• 


Fig.  7.  Si.v  /briHS  of  streptococci,  i.  Long  chains  consisting  oj 
small  segments  arranged  ivith  equal  spaces  beliveen  them.  2.  Long  and 
shorter  chains  in  ivhich  the  segments  are  arranged  in  pairs.  The  size 
of  the  individual  segmeitts  is  considerably  larger  than  those  in  the  long 
chains,  j.  Short  and  longer  chains  where  the  segments  are  oval  ivith 
the  long  diameter  perpendicular  to  the  long  axis  of  the  chain.  4.  Long 
iTiterlacing  chains.  5.  Short  and  longer  chains  with  one  or  more  seg- 
ments very  much  larger  than  the  others.  6.  Chains  shoiving  divisions 
in  two  planes.  This  form  of  division  has  been  observed  in  a  feiv  cases. 
The  dividing  in  tivo  planes  is  an  exception  xvhich  is  not  satisfactorily 
explained.     X  about  1000. 


40  STREPTOCOCCI 

of  their  description  and  the  failure  of  the  author  to  nientiou 
any  character  or  property,  or  combination  of  the  same,  which 
would  distinguish  it  from  others.  However,  such  deficiencies 
cannot  well  be  avoided  in  the  time  of  rapid  accumulation  ot 
observations  and  the  evolution  of  methods. 

§  20.  Classification  of  streptococci.  A  few  investi- 
gators have  tried  to  eliminate  the  confusion  concerning  species 
by  classifying  streptococci  according  to  distinct  morphologic 
characters  and  pathogenic  properties.  Of  these  classifications 
the  following  may  be  mentioned  : 

I.  The  classification  of  von  Lingelsheim.  This  author  di- 
vides all  streptococci  into  two  groups,  or  species,  namely  :  — 

{a)   Streptococcus  brcvis — which  is  non-pathogenic. 

{b)   Streptococcus  longus — which  is  pathogenic. 

This  is  a  combination  of  pathogenesis  and  morphology 
which  the  author  thought  applicable  to  the  entire  genus.  He 
worked  very  largely,  however,  with  the  streptococci  from  the 
human  mouth  and  throat. 

n.  The  classification  of  Kurth.  Kurth  worked  largely 
with  the  streptococci  from  cases  of  scarlatina.  His  system  is 
practically  the  same  as  that  of  von  Lingelsheim,  with  the  ex- 
ception that  he  does  not  include  pathogenesis  as  necessarily 
belonging  to  either  group.     The  divisions  are  as  follows  : 

{a)  Streptococcus  rigidi — Streptococci  growing  in  short 
chains,  imparting  a  uniform  turbidity  to  bouillon. 

ib)  Streptococcus  flexuosi — Streptococci  which  grow  in 
long  interlacing  chains  forming  flocculi  in  bouillon,  leaving 
the  liquid  clear. 

HI.  The  classification  of  Pasquale.  Pasquale  worked  with 
thirty-three  streptococci,  including  nearly  all  of  the  then 
known  species.  His  work  was  quite  exhaustive,  but  he  had 
to  deal  with  cultures  of  various  generations.  He  divides  them 
into  four  groups,  as  follows  : 

(a)  Short  saphrophytic  streptococci. 


DISTRIBUTION    OF   STREPTOCOCCI  4I 

(d)    Long  non-virulent  streptococci. 

(c)    Long  pathogenic  streptococci. 

i^d)    Short  highly  infectious  streptococci. 

Group  (d)  pertains  largely  to  bacteria  which  are  no  longer 
recognized  as  streptococci,  for  example,  the  diplococcus  {Hficro- 
tocciis  lanceolaftis)  of  pneumonia.  It  is  now  known  that  strep- 
tococci which  grow  in  short  chains  are  often  virulent.  This  is 
especially  true  of  the  pyogenic  forms. 

The  study  of  streptococci  from  various  sources,  more 
especially  from  tissues  of  diseased  animals,  suggests  the  desira- 
bility of  delaying  a  further  classification  until  more  definite 
data  are  obtained  concerning  the  natural  history,  not  only  of 
these,  but  also  of  the  species  normally  present  on  the  mucous 
membranes  of  animals  and  in  nature  generally.  The  specific 
name  is,  pathologically  or  even  biologically  speaking,  of  little 
moment  unless  we  can  attach  a  certain  definite  meaning  to  it 
concerning  the  morphologic  characters,  cultural  manifestations 
and  the  degree  of  disease-producing  power  possessed  by  the 
organism  designated.  In  a  group  of  twenty-eight  streptococci 
previously  studied,  the  writer  found  the  pathogenic  forms, 
i.  e.  those  able  to  produce  disease  in  rabbits,  guinea  pigs,  or 
mice,  about  equally  divided  between  the  long  and  short  chains. 
Of  the  twenty-eight,  nine  possessed  a  certain  amount  of  viru- 
lence for  one  or  more  of  these  animals. 

§  21.  Distribution  of  streptococci  in  nature.  The 
fact  has  been  pointed  out  in  many  publications  that  strepto- 
cocci are  quite  widely  distributed  in  nature.  The  results  of 
the  bacteriologic  examinations  of  normal  mucous  membranes 
show  that  they  are  frequently  included  in  the  bacterial  flora  of 
the  mouth,  throat,  nares,  intestines,  vagina,  and  in  a  few  cases 
they  have  been  found  in  the  bronchioles  of  the  horse  and  rab- 
bit They  are  also  present  in  greater  or  less  numbers  on  the 
skin,  especially  in  the  deeper  layers,  presumably  in  the  ducts 
of  the  sweat  and  sebaceous  glands  and  along  the  hair  shafts 
and  follicles.  They  exist  in  soil  and  in  water,  and  occasionally 
these   forms  are  quite  as  delicate    in    their    morphology    and 


42  STREPTOCOCCI 

equally  as  sensitive  to  the  influence  of  environment  as  those 
isolated  from  diseased  animal  tissues.  In  view  of  this  wide 
distribution,  the  presence  of  a  streptococcus  in  any  abnormal 
condition  cannot  be  considered  necessarily  a  specific  infection 
from  a  previous  case  of  the  same  kind.  In  many  affections 
where  the  specific  organism  has  been  demonstrated,  such  for 
example  as  diphtheria,  tuberculosis  and  hog  cholera,  strepto- 
cocci frequently  appear  m  the  lesions.  In  these  cases,  they 
are  considered  as  accidental  or  secondary  invaders,  although 
in  some  of  these  maladies,  such  as  tuberculosis,  they  are  be- 
lieved to  be  of  more  or  less  secondary  importance.  When,  how- 
ever, the  specific  cause  of  the  disease  is  not  positively  known, 
and  streptococci  which  possess  certain  pathogenic  powers  for 
experimental  animals  are  constantly  present  and  seem  to 
stand  in  a  causal  relation  to  the  disease,  the  pathologist  is 
confronted  with  a  puzzling  problem  in  trying  to  determine  the 
source  and  the  etiological  importance  of  the  organism  in  hand. 
In  cases  of  infection  leading  at  once  to  septicemia,  peritonitis 
or  suppuration,  the  explanation  is  more  simple  than  in  the 
epizootic  diseases,  such  as  Bncsiseuche,  where  the  constant 
presence  of  streptococci  in  the  lesions  can  be  quite  as  easily 
explained  on  the  ground  of  their  invasion  of  the  parts  affected 
from  a  normal  habitat  as  on  the  hypothesis  of  a  specific  in- 
fection. It  is  in  these  instances  that  we  are  seeking  for  the 
crucial  test. 

We  have  found  in  a  few  test  experiments  that  when  cer- 
tain of  the  delicate  streptococci  which  exist  (are  found;  in  ex- 
ternal nature  (soil  or  water)  are  introduced  within  the  tissues 
of  certain  animals  they  become,  by  reason  of  their  activities,  a 
source  of  irritation  which  causes  local  tissue  disturbances.  In 
a  few  cases  they  have  produced  septicemia  with  fatal  results. 

In  cases  of  infection  resulting  in  septicemia,  or  in  those 
where  the  disease  is  more  localized,  as  in  strangles  or  mastitis, 
and  possibly  in  others  where  the  affection  spreads  more  or  less 
rapidly,  we  cannot  well  escape  from  the  feeling  that  the  strep- 
tococci, present  in  such  large  numbers,  must  either  stand  in  a 
causal  relation  to  the  disease   or   be   accounted    for    bv    their 


DISTKIHUTION     OF    STKRI'TOCOCCI  43 

rapid  proliferation  in  native  soil  made  favorable  for  their  ex- 
cessive increase  by  the  conditions  produced  by  the  true  etio- 
logical factors.  Their  natural  distribution  is  so  wide  and 
their  virulence  so  capricious  that  a  secondary  invasion,  which 
seems  always  to  be  possible,  renders  the  fixing  of  etiological 
responsibility  upon  a  streptococcus  isolated  from  any  diseased 
tissue  a  somewhat  difficult  task.  The  problems  in  this  con- 
nection which  concern  us  most  and  which  need  more  extended 
investigation  pertain  (i)  to  the  determination  of  the  parasitic 
possibilities  of  streptococci  existing  in  nature,  /.  e.,  those  ordi- 
narily considered  as  saprophytes  and  (2)  to  the  distinction,  if 
it  exists,  between  streptococci  that  are  able  to  produce  local 
inflammatory  processes  leading  to  suppuration  and  those  which 
produce  highly  infective  and  rapidly  spreading  diseases,  such 
as  erysipelas  and  strangles. 

In  view  of  the  confusion  respecting  species  in  this  genus, 
the  identity  of  streptococci  isolated  from  the  lesions  in  the 
various  diseases  which  have  been  attributed  to  streptococci  is, 
at  the  present  time,  a  matter  of  some  uncertainty.  There  is 
also  considerable  skepticism  concerning  the  primary  etiological 
significance  of  the  streptococci  in  a  number  of  diseases  in 
which  they  have,  heretofore,  been  assigned  as  the  cause. 
Recent  investigations,  especially  those  of  Lignieres,  tend  to 
the  conclusion  that  they  are  often  secondary  invaders  in  cer- 
tain of  these  diseases.  Petruschky  has  pointed  out  analogous 
cases  in  human  infections  in  showing  that  streptococci  play  an 
important  role  as  secondary  invaders  in  human  diphtheria, 
scarlatina  and  tuberculosis. 

Pathogeyiesis.  In  the  absence  of  verified  results  to  prove 
the  non-specific  relation  of  streptococci  to  the  diseases  which 
have  with  reasonable  certainty  been  attributed  to  the  activities 
of  this  genus  of  bacteria,  these  affections  are  tentatively 
included  among  the  specific  streptococcic  maladies.  It  is  very 
important,  especially  when  the  use  of  antistreptococcic  serums 
are  in  question,  to  take  into  account  the  apparently  large 
number  of  forms,  or  species,  commonly  included  in  the  general 
statement  of  a  streptococcus   disease   or    infection.      In    1S97, 


44  STRANGLES 

Van  de  \^elde,  in  a  very  exhaustive  series  of  experiments, 
showed  that  an  antitoxin  produced  from  one  streptococcus  will 
not  immunize  against  another,  save  to  a  very  slight  degree. 
Better  results  are  reported  by  the  use  of  polyvalent  serums. 
There  are  a  number  of  acute  local  disorders,  such  as 
vaginitis  in  cows,  that  have  been  attributed  to  this  genus. 

REFEREXCES. 

1.  Klein.  Seventeenth  Annual  Report  of  the  Local  Government 
Board.  Supplement  containing  report  of  Medical  Officer.  London. 
1887,  p.  256. 

2.  KuRTH.  Arbeiten  a.d.  Kaiserlichen  Gesundhcitsamte,  Bd.  VII 
(i89i),S.  389. 

3.  Moore.  Bulletin  No.  j.  U.  S.  Bureau  of  Animal  Industry, 
1893.  P-  9- 

4.  Pasquale.  Beitriige  zur  path.  Anal.  u.  zur  allgemeinen 
Palhologie,  Bd.  XII  (1893),  S.  433. 

5.  Petruschky.     Zeitschrijtf.  Hygiene,  Bd.  XVII,  S.  59. 

6.  VON  LiNGELSHEiM.  Zeitschrift  f.  Hygiene,  Bd.  X  (1891), 
S.  331- 

7.  Welch.  The  Amer.  Jour,  of  Med.  Sciences,  VoL  CII  (1891), 
P-  439- 


vSTRANGLES. 


Synonyms.  Adenitis  equorum  ;  Coryza  contagiosa 
equorum  ;   Distemper:   Goiirme ;  Druse. 

§  22.  Characterization.  Strangles  is  an  infectious  dis- 
ease of  horses,  asses  and  their  hybrids  occurring  sporadically 
and  in  epizootics.  It  is  characterized  principally  by  a  fever, 
followed  by  an  acute  catarrh  of  the  mucosa  of  the  upper  air 
passages  especially  of  the  nares,  and  a  suppurative  inflamma- 
tion of  the  lymph  glands  of  the  submaxillary  and  pharyngeal 
regions.  The  lesions,  however,  are  not  restricted  to  these 
parts.      It  is  a  disease  of  young  animals. 

v^  23,  History.  Strangles  was  among  the  first  equine 
diseases  to  be  recognized.  In  1664,  Solleysel  gives  an  account 
of  it  and  points  to  the  fact  that  it  had  been  known   for  a  long 


HISTORY    OF    STRANGLES  45 

time.  Its  infectious  (contagious)  nature  was  determined 
experimentally  in  1790  by  Lafosse  and  since  that  time  by  a 
number  of  other  investigators.  In  1873,  Rivolta  found  in  the 
pus  of  the  abscesses  a  micrococcus  which  appeared  in  chains  of 
from  three  to  five  segments.  Baruchello,  in  1887,  described 
as  its  cause  an  organism,  which  he  designated  as  Bacillus 
adenitis  eqiii.  Strangles  has  been  thought  by  some  to  be 
identical  with  scrofula  and  measles.  Sacco  and  Nasbot  con- 
sidered it  as  horse  pox.  Viborg  and  Toggia  and  more  recently 
Nasbot  advocated  the  inoculation  of  horses  with  the  lymph  of 
horse  pox  as  a  prophylactic  measure  against  strangles.  Dela- 
motte  demonstrated  that  this  procedure  was  of  little  or  no  pre- 
ventive value.  The  supposed  specific  cause  ^Streptococcus  equi) 
of  strangles  was  described  first  by  Schiitz  and  later  by  Sand 
and  Jensen  in  the  same  year  (1888).  This  discovery  has  been 
confirmed  by  Poels,  Lupka  and  others.  More  recently  Lig- 
nieres  has  discovered  a  "  coccobacillus  "  which  he  believes  to 
be  the  primary  cause.  He  considers  the  streptococcus  of 
Schiitz  as  a  secondary  invader  of  no  specific  value.  His  con- 
clusions do  not  appear  to  have  been  confirmed. 

§  24.  Geographical  distribution.  Strangles  is  a  wide 
spread  disease  among  horses.  It  appears  to  stand  in  equine 
pathology  very  much  as  measles  do  in  human  medicine, — a 
disease  of  early  life  and  consequently  more  prevalent  where 
there  are  more  young.  It  seems  to  exist  in  all  countries 
where  the  horse  kind  are  raised  and  to  be  more  prevalent  in 
breeding  districts  than  elsewhere. 

§  25.  Etiology.  Strangles  is  caused  by  Streptococcus 
equi,  first  described  by  Schiitz  in  1888.  With  pure  cultures  of 
this  organism  Schiitz  was  able  to  produce  the  disease  in 
healthy  horses.  It  is  fatal  to  mice,  a  maximum  virulent  virus 
destroying  life  in  three  days.  In  the  writer's  experience 
streptococci  only  have  been  found  in  the  abscesses. 

The  period  of  ivcubation  varies,  from  four  to  eight  days  is 
the  most  usual  time. 

J;   26.     Symptoms.     The  first  indication  of  this  disease 


46  STRANGLES 

is  a  rise  of  temperature.  There  is  loss  of  appetite,  depression, 
and  often  great  weakness.  The  general  symptoms  may  con- 
tinue for  a  few  days  before  the  localization  of  the  lesions  is 
apparent.  The  first  local  manifestation  consists  usually  in  a 
catarrh  of  the  nasal  mucosa  or  swelling  of  the  sub-maxillary 
and  pharyngeal  lymphatic  glands.  The  nasal  discharge  is  at 
first  serous  and  somewhat  viscid,  but  in  from  3  to  5  days  it  be- 
comes purulent  and  of  a  yellowish  green  color.  The  catarrhal 
condition  may  exist  in  one  or  both  nostrils.  It  may  extend 
into  the  pharynx,  larynx,  trachea  and  even  to  the  bronchi.  In 
most  cases,  swelling  of  the  sub- maxillary  glands  appears  con- 
currently with  the  purulent  nasal  catarrh.  The  spreading  of 
the  inflammation  to  the  connective  tissue  which  surrounds  the 
glands,  and  the  stasis  of  the  lymph  in  the  efferent  lymph 
vessels,  often  cause  the  development,  from  the  sub-maxillary 
lymph  glands,  of  very  extensive  swellings  that  may  occupy 
the  entire  inter-maxillary  space,  and  may  spread  even  to  the 
outer  side  of  the  maxilla.     Abscesses  form  in  most  cases. 

In  exceptional  cases,  strangles  may  present  catarrhal 
symptoms  without  suppuration  of  the  lymph  glands.  Jensen 
states  that  it  may  first  assume  the  form  of  pharyngitis,  purulent 
pneumonia,  and  pleuritis  without  any  well  marked  morbid 
affection  of  the  lymph  glands.  The  urine  generally  remains 
alkaline  ;  it  frequently  contains  a  considerable  quantity  of 
albumen. 

At  times,  strangles  is  accompanied  by  a  cutaneous  exan- 
thema which  takes  the  form  of  an  eruption  of  w^heals,  nodules, 
vesicles  and  even  pustules  ;  these  may  appear,  chiefly  on  the 
sides  of  the  neck,  shoulders  and  sides  of  the  chest.  These 
exanthemata  are  characterized  by  their  sudden  appearance, 
and  often  by  their  equally  rapid  disappearance.  An  eruption 
of  vesicles  may  break  out  on  the  nasal  mucous  membrane. 
The  contents  of  the  vesicles  is  at  first  limpid,  but  later  it 
becomes  purulent.  Rabe  states  that  the  streptococcus  of 
strangles  can  produce  ulcers  on  the  nasal  mucous  membrane. 

§  27.     Morbid  anatomy.     The  lesions  in  strangles  are 


MORBID    ANATOMY 


47 


interesting  from  the  fact  that  in  the  beginning  the  disease  is 
general  but  later  in  its  course  it  becomes  a  series,  exceedingly 
variable  in  different  individuals,  of  localized  morbid  foci. 
The  lymphatic  glands  seem  to  suffer  most,  although  any  organ 
may  be  involved.  As  indicated  by  the  symptoms,  the  lesions 
in  most  cases  are  characterized  by  an  acute  inflammatory  pro- 
cess followed  by  suppuration. 

The  glandular  swellings  about  the  head  usually  terminate 
in  suppuration,  the  pus  discharging  either  externally  or  into 
the  oral  cavity.  In  other  cases  the  pus  undergoes  caseation. 
Frequently  the  inflamed  glands  become  confluent,  resulting  in 
a  single  large  abscess.  Small  abscesses  may  occur  under  the 
pharyngeal  mucosa. 

The  inflammation  may  extend  to  the  superficial  lymph 
vessels  of  the  skin,  especially  of  the  head,  resulting  in  the  for- 
mation of  a  large  number  of  small  abscesses.  This  may  be 
followed  by  a  diffuse  phlegmonous  swelling  of  the  parts. 
Metastatic  abscesses  are  liable  to  occur  in  a  great  variety  of 
organs.  The  metastasis  seems  to  take  place  through  both 
lymph  and  blood  vessels  although  the  lymphatic  glands  are 
most  often  affected.  Suppurating  foci  have  been  described  in 
nearly  every  lymphatic  gland  in  the  body.  The  discharge  of 
pus  from  the  bronchial,  mesenteric  or  other  glands,  within  or 
adjacent  to  the  pleura  or  peritoneal  cavities,  may  give  rise  to 
a  fatal  pleuritis  or  peritonitis.  There  is  no  organ  of  the  body 
free  from  possible  suppurative  lesions  as  a  result  of  metastasis. 

Strangles  may  become  chronic,  especially  when  the  nasal 
catarrh  extends  into  the  sinuses  of  the  head,  in  the  guttural 
pouches,  or  pharyngeal  cavity.  In  these  cases  the  animal  be- 
comes emaciated.  The  lesions  in  these  cases  resemble  some- 
what those  of  chronic  glanders.  Many  complications  are 
liable  to  arise.  Mixed  infections  and  secondary  lesions  often 
occur.     The  prognosis,  however,  is  favorable. 

Death  from  strangles  is  caused  usually  by  either  septi- 
cemia, pyemia,  pleuritis,  peritonitis  or  suppurating  (metas- 
tatic) pneumonia. 

The  duration  of  the  disease  varies  according  to  its  .severity 


48  STRANGLEvS 

and  the  localization  of  the  lesions.  In  mild  cases  conva- 
lescence begins  in  a  few  days,  but  in  other  cases  restoration 
may  require  weeks  and  even  months. 

The  mortality,  according  to  available  statistics,  does  not 
exceed  three  per  cent. 

i<  28.  Differential  diagnosis.  Strangles  is  to  be  differ- 
entiated from  : 

1  Purulent  nasal  eatarrh.  In  this  affection,  there  is 
rarely  suppurating  sub-maxillary  glands,  although  occasional- 
ly these  glands  may  be  swollen. 

2  Glanders.  In  glanders,  the  tissue  changes  are  more 
persistent  and  the  skin  lesions,  if  they  exist,  do  not  heal  as 
rapidly  as  in  strangles.  In  chronic  cases,  the  diagnosis  is 
quite  difficult.  Here  animal  inoculation  must  be  resorted  to. 
Mice  inoculated  subcutaneously  with  the  nasal,  discharge  suc- 
cumb to  the  streptococcus  of  strangles  but  they  are  resistant 
to  the  bacterium  of  glanders.  Guinea  pigs  inoculated  in  a  like 
manner  will,  in  case  of  glanders,  develop  that  disease  from 
the  lesions  of  which  pure  cultures  oi  Baeterium  mallei  may  be 
obtained. 

3  Parotiditis.  In  this  affection  the  swelling  is  localized 
and  suppuration  does  not  often  occur. 

4  Abscesses  due  to  pyogenic  bacteria.  The  cases  are  rare 
where  there  would  be  any  question  as  to  diagnosis.  The  bac- 
teriological examination  including  the  inoculation  of  animals 
would  give  positive  aid  unless  the  pyogenic  organism  hap- 
pened to  be  a  virulent  streptococcus  in  which  case  a  differen- 
tiation might  be  difficult. 

§  29.  Prevention.  Isolation  of  the  infected  and  removal 
of  healthy  animals  from  the  place  where  the  diseased  animals 
came  down.  If  in  stables  the  stalls  should  be  thoroughly 
disinfected  before  being  used  for  well  animals. 

REFERENCES. 
I.     LiGNiERES      The  etiology  of    equine    influenza    as    infectious 
pneumonia.    Jour.  Compr.  Patli.  and   Thera.,  Vol.  XI  {iSgS),  p.  312. 
Translated  from  Recueil  de  Med.  Vet.,  Vol.  IV   (1897). 


EQUINE    PLEURO-PNEUMONIA 


49 


2.  Poles.     Die  Mikrokokken    der   Druse    des  Pferdes.     Forischr. 
der  Med.,  Bd.  VI  (1888),  S.  4. 

3.  Reeks.      Intracranial    strangles,    abscess    in    a    mare.     Jour. 
Compr.  Path,  and  T/iera.,     Vol.  XII  (1899),  p.  178. 

4.  Sand  and  Jensen.     Die  Aetiologie  des  Druse.     Deutsche  Zeit. 
fur  Thiermed.,  Bd.  XIII  (1888),  S.  437. 

5.  ScHUTz.     Der  Streptococcus  der  Druse  des  Pferdes.     Arch,  fur 
Thierheilkunde,  Bd.  XIV  (1888),  S.  172. 


EQUINE  CONTAGIOUS  PLEURO  PNEUMONIA. 

Synonyms.  Pleuro-pneumouia  contagiosa  equorum ;  stable 
pneumonia;  pjieninoenteritis;    Bnistsenc/ie. 

ij  30.  Characterization.  This  disease  known  as  conta- 
gious pneumonia  or  contagious  pleuro-pneumonia  in  the  horse 
is  characterized  by  a  high  temperature,  rapid  pulse,  but  occa- 
sionally without  definite  lung  disturbances.  Like  strangles, 
both  the  symptoms  and  the  lesions  vary  to  such  a  degree  that 
it  is  difficult  to  single  out  diagnostic  features. 

§  31.  History.  In  earlier  times,  influenza  and  conta- 
gious pleuro-pneumonia  of  the  horse  were  not  distinguished  as 
separate  diseases.  Falke  differentiated  the  disease  formerly 
known  as  influenza  into  contagious  pleuro-pneumonia  and 
influenza.  Since  his  time  they  have  been  recognized  as  dis- 
tinct diseases. 

>j  32.  Geographical  distribution.  Contagious  pneu- 
monia, like  strangles,  is  widely  distributed.  It  appears  in  epi- 
zootic form,  although  in  certain  places  it  is  reported  to  be 
almost  enzootic.  It  prevails  most  extensively  where  large 
numbers  of  horses  are  congregated.  It  has  frequently  been 
reported  as  the  cause  of  much  trouble  among  the  horses  in  the 
European  armies.  In  the  eastern  part  of  the  United  States,  it 
appears  from  time  to  time  in  more  or  less  serious  epizootics. 
It  is  quite  common  among  horses  shipped  from  the  West.  In 
these  cases,  it  is  designated  as  "western"  or  "stable"'  fever. 


50  EQUINE    PLEURO--PNEUMONIA 

>5  33.  Etiology.  There  is  some  question  concerning  the 
specific  cause  of  this  disease.  A  large  number  of  suspected 
microorganisms  have  been  isolated  and  described,  but  the 
streptococcus  of  Schiitz  seems  to  be  the  only  one  with  which 
the  disease  has  been  produced  experimentally. 

In  1887,  Schiitz  published  the  results  of  his  investigations 
into  the  cause  of  BrustseMche.  He  described  an  organism 
which  appeared  as  a  diplococcus  in  tissues,  but  in  bouillon 
cultures  it  grew  in  flocculi.  From  the  description,  it  appears 
that  this  organism  was  a  streptococcus,  notwithstanding  the 
fact  that  in  the  tissues  it  appeared  more  often  as  a  diplococcus. 
In  cultures,  he  speaks  of  it  as  chains  growing  in  masses.  He 
mentions  a  capsule,  but  in  the  cases  described  it  does  not  seem 
to  be  invariably  present  and  it  is  not  mentioned  in  prepara- 
tions made  from  cultures.  Chantemesse  and  Delamotte,  Gal- 
tier  and  Violet,  and  Cadeac  found  streptococci  in  the  lesions 
of  animals  suffering  from  this  disease.  Although  differences 
seem  to  exist  in  the  streptococci  isolated  and  studied  by  these 
investigators,  there  is  a  striking  similarity  between  them.  It 
is  not  at  all  unlikely  that  difference  in  methods  may  explain 
the  variations  mentioned. 

According  to  Schiitz,  cultures  inoculated  into  horses  pro- 
duce the  disease  when  injected  directly  into  the  lungs  by 
means  of  a  hypodermic  syringe.  The  resulting  contagious 
pleuro-pneumonia  exhibits  the  same  symptoms  and  runs  a  like 
course  to  those  observed  in  cases  of  the  disease  contracted  in 
the  natural  or  common  manner.  The  essential  changes  shown 
on  post-mortem  examination  were  multiple  gangrenous  patches 
in  the  lungs  with  parenchymatous  degeneration  of  the  most 
important  organs.  The  inoculated  streptococci  were  found  in 
the  tissues  of  the  artificially  produced  disease.  According  to 
Schiitz,  the  bacteria  of  contagious  pleuro-pneumonia  are  found 
most  numerously  in  the  lungs  or  the  exudate  on  the  pleurae. 
They  are  also  met  with  in  the  nasal  discharge  and  in  expired 
air  (Rust).  Nothing  positive  is  known  concerning  the  life 
history  of  the  streptococci  outside  the  animal  body.  They  are 
supposed  not  to  be  able  to  live  longer  than   six  weeks  within 


i-:tiology  51 

the  animal  body  ;  but  in  certain  cases,  especially  in  encysted 
deposits  in  the  lungs,  the  virus  may  remain  active  for  a  much 
longer  time. 

Baumgarten  and  Hell  oppose  the  view  that  Schiit/.'s  strep- 
tococcus is  specific,  while  Rust  and  Fiedler  support  it.  Hell 
maintains  that  with  our  present  means  of  investigation,  the 
bacteria  of  contagious  pleuro-pneumonia  cannot  be  differen- 
tiated from  the  pyogenic  streptococci  or  from  the  strepto- 
coccus of  erysipelas  In  fact,  Hell  believes  that  the  strepto- 
coccus of  Schiitz  has  a  pathogenic  effect  in  horses  affected 
with  pleuro-pneumonia  ;  but  as  there  is  no  positive  proof  of 
its  being  specific,  he  maintains  that  we  are  justified  in  sup- 
posing that  this  ubiquitous  microorganism  simply  has  an  injuri- 
ous influence  on  the  course  of  the  disease,  contributing  to  the 
production  of  the  secondary  lesions.  Hell  further  states  that 
protective  inoculation  with  Schiitz's  bacteria,  which  at  first 
promised  good  results,  has  not  proven  to  be  satisfactory. 
Fiedler,  on  the  other  hand,  has  obtained  the  same  bacteriolog- 
ical results  and  has  arrived  at  the  same  conclusion  as  Schiitz. 
He  also  states  that  he  has  experimentally  produced  pleuro- 
pneumonia in  a  horse  by  inoculation  of  cultivations  of  these 
bacteria. 

Lignieres  believes  that  his  cocco-bacillus  stands  in  an 
etiological  relation  to  this  disease  and  that  here,  as  in  strangles, 
the  streptococcus  is  a  secondary  invader.  This  view  has  not 
been  confirmed. 

The  writer  made  a  bacteriological  examination  of  the 
organs  from  five  cases  of  fatal  contagious  pneumonia  of  the 
horse.  In  each  case,  the  lungs  were  more  or  less  hepatized, 
but  the  other  organs  were  nearly  normal  in  appearance. 
Without  exception,  a  streptococcus  appeared,  usually  in  pure 
culture,  from  the  lungs.  The  inoculated  media  from  the  other 
organs  (liver,  spleen,  and  kidney)  remained  clear.  The  strep- 
tococci isolated  from  the  different  cases  were  identical  in 
their  morphology,  cultural  manifestations  and  pathogenesis. 
A  microscopic  study  of  the  lungs  from  the  different  horses 
showed  streptococci  singly,  in  pairs  and  occasionally   in  short 


52  EOUINK    PLEURO-PNEUMONIA 

chains.  Distinct  capsules  were  not  observed.  In  bouillon 
cultures,  however.  the\'  appeared  in  long  chains,  leaving  the 
liquid  clear,  as  described  by  Schiitz. 

This  streptococcus  did  not  grow  in  gelatin,  or  on  serum, 
or  on  potato.  It  would  not  develop  in  acid  media.  On  agar 
the  colonies  were  small  and  characteristic  of  streptococci,  i.  e., 
with  a  thickened,  convex,  grayish  center  surrounded  by  a 
thin,  spreading  bluish  border,  nearly  equal  in  width  to  the 
diameter  of  the  central  portion.  It  fermented  dextrose,  lac- 
tose and  saccharose,  with  the  formation  of  acids  but  no  gas. 
Milk  remained  unchanged  in  appearance. 

In  mice  and  rabbits,  it  produced  a  rapidly  fatal  septicemia, 
but  guinea-pigs  were  unaffected.  A  horse  inoculated  in  the 
pleural  cavity  with  a  small  quantity  of  the  culture  was  killed 
lo  days  later.  At  the  point  of  inoculation  and  extending  over 
an  area  equal  to  one-half  of  the  lung,  there  were  strong  adhe- 
sions between  the  lung  and  parietes.  The  subjacent  lung 
tissue  w^as  hepatized.  Pure  cultures  of  the  streptococcus  were 
obtained  from  the  exudate  and  from  the  hepatized  lung. 

Although  a  few  discrepancies  exist  between  the  descrip- 
tion of  Schiitz's  organism  and  this  streptococcus,  in  the  more 
essential  features  they  seem  to  be  identical.  The  cases  were 
examined  before  the  publication  of  Lignieres'  results,  and  the 
methods  employed  did  not  meet  the  requirements  of  those  used 
in  isolating  his  cocco-bacillus.  Although  a  very  careful  histo- 
logical study  of  the  pneumonic  tissue  was  made,  Ligniere's 
organism  was  not  detected.  It  is  known  that  a  bacterium, 
resembling  that  described  by  Lignieres,  exists  normally  in  the 
upper  air  passages  of  a  certain  number  of  horses. 

The  period  or  inriibation  is  g\y&\\  as  varying  from  one  to 
fourteen  days,  but  usualh-  from  lour  to  ten   days  elapse   from 

the  time  of  exposure  to  the  development  of  the  first  symptoms. 

^  34.  Symptoms.  The  symptoms  vary  to  a  marked  de- 
gree. When  pneumonia  develops  early  in  its  course,  the  dis- 
ease may  appear  suddenly  ;  and  in  addition  to  the  elevation  of 
temperature  there  is  a  cough  with  difficult  breathing.     Often 


SYMPTOMS  53 


the  svraptoms  differ  from  those  of  fibrinous  pneumonia  by  the 
absence  of  distinct  evidences  of  local  lesions  which  are  found 
in  that  disease.  The  first  regular  symptom  is  a  rapidly 
increasing  temperature  frequently  accompanied  by  a  chill.  The 
pulse  rate  is  increased.  There  is  general  depression,  usually 
lossof  appetite  and  muscular  weakness;  the  conjunctivae  and 
other  visible  raucous  membranes  become  congested.  There 
may  be  from  the  beginning  marked  indications  of  localized 
lesions  in  the  lungs,  or  the  general  symptoms  may  continue 
without  evidence  of  pronounced  lung  disturbance.  The  dura- 
tion of  the  disease  depends  almost  entirely  upon  its  course. 
In  the  more  tvpical  cases,  the  fever  lasts  from  5  to  8  days. 
The  period  of  convalescence  is  much  longer,  lasting  from  two 
to  three  weeks.  Many  symptoms  may  be  exhibited,  corres- 
ponding to  the  variations  in  the  morbid  processes.  If  the 
heart,  digestive  tract,  liver,  kidneys  or  brain  become  the  local- 
ized seat  of  the  disease,  symptoms  referable  to  impaired  func- 
tions of  these  organs  are  in  evidence.  The  septicemic  form 
has  been  described  as  being  followed  by  localized  suppurative 
lesions. 

§  35.  Morbid  anatomy.  The  morbid  changes  in  the 
tissues  and  organs  vary  according  to  the  course  of  the  disease, 
which  is  exceedingly  irregular.  It  may  exhibit  a  regular 
form  of  lobar  inflamation  of  the  lungs  or  the  disease  may  run 
an  atvpical,  complicated,  acute,  chronic,  and  not  infrequently 
an  abortive  course.  Further,  authorities  agree  that  many  com- 
plications mav  arise  modifying  or  changing  completely  the 
morbid  anatomv  of  the  disease  from  the  conditions  found  m 
the  more  tvpical  cases.  In  the  few  cases  examined  post-mor- 
tem by  the  writer,  the  gross  lesions  were  restricted  to  the  lungs. 
They  were  either  in  a  state  of  congestion,  or  exhibited 
changes  of  fibrinous  pneumonia  in  the  cephahc  (anterior) 
portions  of  one  or  both  organs.  Pneumonia  is  the  most  com- 
mon localized  lesion.  Several  quite  distinct  forms  of  lung 
disturbances  are  described. 

In    the    lobular    form    of    pleuro-pneumonia.    which  it  is 


54  EQUINE  PLEURO- PNEUMONIA 

Stated  furnishes  the  largest  number  of  subjects  for  post-mortem 
examination,  there  are  many  hemorrhagic  foci,  possibly  gan- 
grenous pneumonia  with  secondary  pleuritis.  Parenchymatous 
degeneration  of  other  vital  organs  is  reported.  Areas  of  the 
lung  tissue  of  greater  or  less  size  are  thickened  and  hepatized- 
These  are  located  more  especially  near  the  base  of  the  lungs 
and  in  the  lower  (ventral)  portions.  Bright  foci  which  are 
distinctly  defined  from  the  neighboring  tissues  are  scattered 
through  the  hepatized  areas  and  appear  on  the  surface  of  sec- 
tions of  the  hepatized  parts.  Uusually  several  of  these  foci 
are  present.  They  vary  in  size  from  a  millimeter  to  20  or 
more  centimeters  in  diameter.  In  recent  lesions,  these  areas 
are  very  small,  of  a  grayish-red  color  and  surrounded  by  a 
grayish  zone  consisting  of  leucocytes.  In  more  advanced 
lesions  they  become  yellowish,  necrotic  and  finally  cavities 
are  formed  varying  from  the  size  of  a  pea  to  that  of  a  hen's 
egg.  These  cavities  are  surrounded  by  a  smooth  capsule. 
There  are  other  foci  which  contain  greasy,  fetid,  watery  pus 
(gangrene  of  the  lungs),  by  reason  of  the  necrotic  part  of  the 
lung  undergoing  liquefaction  in  consequence,  it  is  stated,  of 
the  admittance  of  air.  The  lungs  often  contain  suppurating 
foci  composed  of  a  whitish  pus  mixed  with  necrotic  lung 
tissue.  It  sometimes  happens  that  the  foci  just  described  are 
absent  in  the  lungs,  although  during  life  distinct  symptoms 
of  such  a  localized  affection  may  have  been  present.  In  these 
cases,  it  is  assumed  that  absorption  of  the  necrotic  tissue  has 
taken  place.  The  remaining  tissue  of  the  lungs  is  more  or 
less  hyperemic  or  edematous. 

The  pleurae  show  signs  of  a  difi'use,  exudative  inflamma- 
tion, the  starting  point  of  which  in  the  large  majority  of  cases 
is  from  necrotic  deposits  which  are  situated  in  the  periphery 
of  the  lungs.  Pleuritis  may  occur,  however,  apparently  as  a 
primary  lesion  without  the  necrotic  foci  being  present.  The 
contents  of  a  necrotic  deposit  in  the  lungs  rarely  break 
through  into  the  pleural  cavity.  In  some  cases,  the  visceral 
and  costal  layers  of  the  pleurae  are  congested,  diffusely  or  in 
spots,  and  are  sprinkled   with   hemorrhages.      Frequently  the 


MORBID    ANATOMY  55 

pleurae  are  covered  with  soft  red  granulations  over  which  are 
layers  of  a  yellowish  exudate  which  are  partly  membranous 
and  partly  coagulated  in  a  reticular  manner,  and  which  can 
usually  be  easily  removed.  The  pleural  cavities  generally 
contain  a  considerable  quantity  of  fluid.  Dieckerhoff  states 
that  from  30-40  liters  of  a  serous  fluid  are  occasionally  present. 
The  exudate  is  usually  turbid  and  of  an  orange,  grayish-red, 
brownish-red,  or  dirty-grayish  color.  It  is  generally  mixed 
with  numerous  yellowish  colored  flakes  which  form  a  sediment 
when  the  liquid  is  allowed  to  stand  in  a  glass.  The  pleuritic 
exudate  sometimes  consists  of  pure  pus  and  less  frequently  of 
blood.  The  pleuritic  exudate  when  present  in  large  amount 
compresses  the  lungs  and  pushes  them  away  from  the  thoracic 
walls.  In  cases  of  recovery,  the  pleuritic  exudate  may  become 
organized,  binding  the  lungs  to  the  costal  walls  and  diaphragm. 
Various  forms  of  fibrous,  villous  growths  develop  on  the 
pleurae. 

The  records  show  that  the  other  organs  of  the  body  are 
usually  in  a  state  of  parenchymatous  inflammation  and  fatty 
degeneration.  The  muscular  tissue  of  the  heart  is,  as  a  rule, 
brownish-gray  in  color,  soft,  and  suffers  from  cloudy  swelling. 
In  severe  cases,  it  shows  well-marked  fatty  degeneration,  is  of 
a  clay  color,  and  is  occasionally  sprinkled  with  a  large  number 
of  small,  yellowish-white  foci.  The  liver  is  enlarged,  of  a 
clay  color  or  sometimes  icteric,  and  presents  signs  of  fatty 
degeneration.  The  spleen  is  flaccid,  its  pulp  increased  and 
often  sprinkled  with  hemorrhages.  The  kidneys  may  be  swollen, 
friable  and  sometimes  show  numerous  hemorrhagic  foci. 
The  lymph  glands,  especially  the  bronchial  and  mediastinal 
glands,  are  enlarged,  softened,  and  exhibit  on  section  a  grayish- 
red  color.  The  muscles  of  the  body  are  soit,  and  of  a  yellow- 
ish-brown color.  Small  hemorrhages  under  the  serous  mem- 
branes are  frequently  reported.  Slight  endocarditis  may  occur. 
The  blood  suffers  less  change  than  any  of  the  solid  organs. 
It  contains  an  excess  of  polynuclear  leucocytes. 

The  mucous  membranes  of  the  stomach  and  intestines  are 
frequently  hyperemic,  swollen,   sprinkled   with   hemorrhages, 


56  EQUINE    PLEURO-PXEUMOXIA 

and  sometimes  even  ulcerated.  The  bronchial  mucous  mem- 
brane is  swollen  and  inflamed. 

In  other  cases,  the  lesions  are  those  of  lobar  pneumonia, 
in  which  the  stages  of  hyperemia,  red  hepatization,  gray  hepa- 
tization and  resolution  fin  favorable  cases)  follow  each  other 
in  regular  order.  In  a  fatal  case  post-mortemed  by  the  writer 
the  right  lung  was  entirely  involved,  the  left  one  being  but 
slightly  hyperemic.  In  non-fatal  cases,  the  crisis  is  reached 
on  the  5th  or  6th  day,  after  which  resolution  begins. 

As  already  stated  the  lesions  in  this  disease  are  so  ex- 
ceedingly variable  that,  in  addition  to  the  more  typical  pneu- 
monia, almost  any  modification  can  be  found.  The  detailed 
description  of  many  of  these  variations  as  described  by  Dieck- 
erhoff  are  worthy  of  careful  study. 

T/ir  duratio7i  of  the  disease  is  from  two  to  three  weeks.  If 
there  are  complications  the  course  may  be  much  longer. 

The  mortality  is  often  very  high.  The  literature  shows  it 
to  vary  from  one  to  thirty  per  cent.  It  frequently  leaves  ani- 
mals practically  worthless  because  of  pleural  adhesions  and 
other  complications. 

§  36.  Differential  Diagnosis.  This  disease  is  to  be 
differentiated  from  several  disorders. 

1.  Influenza.  In  the  general  form,  where  the  localiza- 
tion of  the  lesions  in  the  lungs  does  not  occur,  it  is  often  con- 
fused with  influenza. 

2.  Bronchial  pneumonia.  The  pneumonia  which  often 
follows  colds  must  be  differentiated  from  the  epizootic  form. 

3.  Aspiration  pneumonia.  The  pneumonia  following  the 
introduction  of  foreign  substances  into  the  lungs,  as  often 
happens  in  giving  medicines,  must  be  distinguished.  The 
history,  course  of  the  disease,  and  the  spread  to  other  animals 
will  do  much  to  settle  the  diagnosis.  In  case  of  post-mortem, 
streptococci  are  often  found  in  all  the  pneumonias.  We  have 
no  positive  lesion  or  organism  by  which  to  determine  the 
diagnosis. 

§  37.     Prevention.     The  short  period  of  incubation  and 


SEPTICKMIA  IN  CHICK.KN.S  57 

the  high  temperature  as  the  early  symptom  render  it  an 
easy  task  to  detect  the  appearance  of  the  disease.  The  well  ani- 
mals should  if  possible  be  removed  at  once  to  other  stables. 
The  stalls  occupied  by  the  infected  animals  should  be  disinfected 
before  being  used  for  other  animals.  Isolation  and  disinfec- 
tion are  the  important  factors  in  checking  the  spread  of  this, 
as  of  other  infectious  diseases. 

To  prevent  the  introduction  of  this  malady,  all  horses 
brought  from  a  distance  should  be  kept  isolated  for  at  least  a 
week  before  allowing  them  to  come  in  contact  with  the  home 
animals. 

RHKKRKNCKS. 

1.  Cadkac.  Contributions  a  r  etiologie  de  la  pueunionie  conta- 
gieuse  dn  cheval.     Compt.  rend  de  la  Soc.  de  Biol.,   1889,  p.  316. 

2.  Fleminc.  Infectious  pneumonia  of  the  horse.  The  Veteri- 
nary Jour.,  Vol.  XXXIII,  p.  I. 

3.  SCHUTz.  Die  Ursache  der  Brustseuche  der  Pferde.  Vircho7v's 
An-hiv,  Bd.  CVII,  S.  356. 

4.  SCHt^rT/..  Die  genuine  Lungenentziindung  der  Pferde.  Archiv 
fur  wissen.  u.  prak.  Thierlieil/ciiride,  Bd.  VIII. 

5.  SiEDAMGROTZKY.  Ueber  infectiose  Pneumonien  bei  Pferden. 
Deutsche  med.  Wochenschrift,  1882,  vS.  668. 

6.  W1LI.IAMS.  Contagious  pleuro-pneumonia  of  the  horse.  Aiiier. 
Vet.  Reviezv,  Vol.  XVI  (1892^,  p.  301. 


APOPLECTIFORM  SEPTICEMIA  IN  CHICKENS. 

ji  38.  Characterization,  A  rapidly  fatal  septicemia  in 
chickens  caused  by  a  streptococcus. 

§  39.  History.  This  disease  was  recently  discovered 
and  described  by  Norgaard  and  Mohler.  Although  the  symp- 
toms and  lesions  given  correspond  .somewhat  closely  to  those 
mentioned  by  Mazza  and  Rabieux,  there  is  a  marked  differ- 
ence in  the  etiological  factor.  The  newly  discovered  disease 
is  based  upon  the  findings  and  investigations  following  a  single 
epizootic  among  fowls.  Thus  far  it  has  been  identified  in  one 
other  locality. 


58  SEPTICEMIA    IN    CHICKENS 

^  40.  Geographical  distribution.  The  only  locality 
from  which  it  has  been  described  is  Loudoun  Co.,  Va.  It 
was  observed  and  a  few  cases  studied  by  Moore  and  Mack  in 
an  epizootic  among  fowls  in  the  northern  part  of  New  York  in 
1905. 

§  41.  Etiology.  This  disease  is  stated  to  be  due  to  a 
streptococcus  which  grows  in  short  or  longer  chains  with  seg- 
ments varying  from  0.6  to  o.8/<  in  diameter.  In  some  cases 
elongated  forms  are  observed.  It  is  an  aerobe,  and  a  faculta- 
tive anaerobe.  When  cultivated  on  artificial  media  it  does  not 
liquefy  gelatin,  it  does  not  change  the  appearance  of  milk,  but 
causes  slight  acidity  and  thickening  of  the  lower  stratum  with- 
out coagulation  of  the  casein.  The  reaction  of  alkaline  bouillon 
is  changed  to  an  acid  one.  It  does  not  give  a  visible  growth 
on  potato.  It  stains  by  Gram's  and  Gram-Weigert's  methods. 
In  bouillon  it  grows  in  somewhat  flaky  masses  while  the 
medium  remains  clear.  It  was  fatal  to  fowls,  mice,  rabbits 
and  swine  ;  guinea  pigs,  dogs  and  sheep  were  not  destroyed 
by  inoculation.   This  organism  has  not  been  specifically  named. 

^  42.  Symptoms.  It  is  not  at  all  uncommon  to  find  the 
fowls  dead  and  lying  under  the  roosts.  Occasionally  capons 
were  observed  to  be  sick  for  from  12  to  24  hours  prior  to 
death.  In  these  cases  the  feathers  become  ruffled  and  the  fowl 
showed  evidence  of  extreme  depression.  The  onset  of  the 
disease  is  very  sudden  and  its  course  a  very  rapid  one,  usually 
terminating  in  death. 

§  43.  Morbid  anatomy.  The  authors  describe  the 
morbid  anatomy  as  follows  :  "The  spleen  is  more  or  less  en- 
larged, showing  hyperplasia  of  the  Malpighian  corpuscles.  The 
pulp  contains  numerous  areas  of  extravasated  blood.  When  a 
stained  section  is  examined  by  means  of  a  hand  lens  a  number 
of  circular  semi-transparent  foci,  the  size  of  a  pin  hole,  may 
be  noted.  These  are  found  on  microscopic  examination  to  be 
centers  of  necrobiosis,  consisting  of  parenchyma  which  has 
undergone  coagulation  necrosis,  and  surrounded  by  a  more  or 


DIFFERENTIAL     DIAGNOSIS  59 

less   well   defined  capsule  of  embryonic  and  further  developed 
connective  tissue  cells  and  filaments. 

"  On  microscopic  examination,  the  kidneys  show  slightly 
swollen  epithelial  cells  of  a  beginning  parenchymatous  degen- 
eration to  well  pronounced  disintegration  of  the  renal 
epithelium  of  acute  nephritis.  The  degree  of  degeneration 
depends,  as  a  rule,  upon  the  course  of  the  disease.  If  a  bird 
succumbs  suddenly  or  in  the  course  of  a  few  hours  the  morbid 
changes  are  either  not  apparent  at  all  or  but  slightly  pro- 
nounced, while,  on  the  other  hand,  the  duration  of  three  or  four 
days  to  a  week  results  in  an  acute  exudative  nephritis.  The 
swollen  or  degenerate  epithelium  of  the  tubules  surrounds  irreg- 
ular masses  of  coagulated  exudate  and  white  blood  corpuscles, 
among  which  are  numerous  short  chains  of  streptococci.  In 
very  acute  cases  with  sudden  death  the  liver  shows  extreme 
hyperemia.  The  cells  have  a  slightly  granular  appearance  in 
addition  to  the  fatty  infiltration  usually  seen  in  the  liver  of 
well  kept  fowls.  When  death  does  not  occur  until  after 
twenty- four  hours  the  liver  cells  also  show  parenchymatous 
or  fatty  degeneration  ;  their  outlines  become  indistinct,  the 
body  very  granular,  and  the  nucleus  takes  the  stain  but 
faintly.  Interlobular  and  intralobular  collections  of  round 
cells  and  leucocytes  appear,  and  in  more  chronic  cases  centers 
of  coagulation  necrosis  may  be  seen.  The  lungs  become 
hepatized.  The  walls  of  the  bronchioles  are  thickened  and  the 
streptococci  may  be  seen  in  the  minute  capillaries.  The  air 
cells  are  filled  with  plasma,  red  blood  corpuscles  and  epithel- 
ium, among  which  the  microorganism  is  easily  detected." 

^  44.  Differential  diagnosis.  This  affection  must  be 
differentiated  from  fowl  typhoid  and  chicken  cholera.  The 
positive  diagnosis  of  each  must  rest  with  the  etiological 
factor.  A  number  of  diseases  of  fowls  have  been  described 
from  various  places  in  Europe  and  Africa,  but  none  of  them 
seem  to  be  caused  by  a  streptococcus. 

§  45.  Prevention.  The  separation  of  the  well  from  the 
diseased  fowls  and  placing  them  in  uninfected  houses  or  yards 


6o  STREPTOCOCCUS    MASTITIS 

is  of  the  first  importance.  Norgaard  and  Mohler  found  that 
immunity  may  be  produced  in  susceptible  animals  by  the 
filtrate  of  bouillon  cultures,  by  sterilized  bouillon  cultures  of 
the  specific  streptococcus,  and  with  the  serum  of  artificially 
immunized  animals. 

REFERENCES. 

Norgaard  and  Mohler.     Apoplectiform  septicemia  in  chickens. 
Bulletin  No.  36,  U.  S.  Bureau  0/  Animal  Industry,  1902. 


vSTREPTOCOCCUS  MASTITLS. 

^46.  Characterization.  The  term  "streptococcus  mas- 
titis" has  been  given  to  an  infectious  disease  of  the  udder  of 
cows  caused  by  a  streptococcus.  It  is  characterized  by  hard 
foci  in  the  gland. 

§  47.  History.  As  early  as  1848,  Brennwold  observed 
in  Switzerland  an  enzootic  mastitis  that  was  difficult  to  cure. 
The  affection  was  called  ''gelber  Gait:'  Since  that  time  this 
affection  has  been  found  in  nearly  all  if  not  all  countries. 
Among  the  more  recent  writers  on  this  subject  may  be  men- 
tioned Hess  and  Borgeand  in  Switzerland,  Nocard  and  Mol- 
lereau  in  France,  and  Zschokke  in  Vienna.  In  America  it 
does  not  appear  to  have  been  studied  independently  of  the 
infectious  form  of  mastitis  described  in  §  17.  The  epizootic 
mastitis  occasionally  reported  in  this  country  may  be  identical 
with  this  supposed  distinctively  specific  disease.  Zschokke 
found  the  streptococcus  in  297  of  the  444  cases  of  altered  milk 
examined. 

§  48.  Geographical  Distribution.  This  affection  has 
been  reported  from  nearly  every  country  where  cows  are  kept. 

§  49.  Etiology.  The  organism  that  causes  this  disease 
was  described  by  Kitt,  as  Streptococcus  agalactia,  and  Guille- 
beau  as  Streptococcus  contagioscc.  It  enters  the  udder  through 
the  ducts  of  the  teats. 

The  writer  has  been  unable  to  differentiate  this  strepto- 


MORBID    ANATOMY  6l 

COCCUS  from  the  one  he  has  found  in  cases  of  mastitis,  and  also 
in  the  milk  of  cows  with  healthy  udders.  Ward  and  Reed 
produced  mastitis  in  a  healthy  udder  with  the  streptococcus 
that  they  had  isolated  from  a  normal  udder. 

The  period  of  incubation  is  very  short,  one  to  three  days  in 
the  produced  cases. 

i^  50.  Symptoms.  The  first  symptom  is  the  diminution 
in  the  quantity  of  milk,  usually  in  but  one  quarter  of  the 
udder.  This  is  quickly  followed  by  indurated  foci  in  the 
affected  glands.  The  part  becomes  inflamed.  The  discharge 
or  secretion  is  thin,  more  or  less  colored,  and  contains  pus 
cells  and  clumps  of  streptococci.  The  lesions  develop  slowly, 
and  one  quarter  after  another  of  the  udder  becomes  involved. 
Later  the  milk  secretion  is  liable  to  stop  entirely. 

§  51.  Morbid  Anatomy.  The  tissue  changes  are 
described  as  those  of  catarrhal  inflammation  of  a  mucous  sur- 
face, followed  by  the  development  of  new  formed  tissue  and 
atrophy  of  the  parenchymatous  tissue.  The  gland  is  hard  and 
in  time  becomes  enlarged,  due  to  the  new  formed  tissue.  The 
microscopic  examination  shows  a  thickened  intertubular 
tissue,  and  the  epithelial  cells  more  or  less  disintegrated  and 
sloughed  from  the  tubular  walls.  The  lymphatic  glands  and 
other  organs  of  the  body  are  not  involved.  The  lesions  are 
localized  in  the  udder. 

The  period  of  duration  is  variable,  but  always  long. 

77z<?/;v^7/(7j^^  is  grave  for  the  gland  itself,  but  is  rarely 
fatal  to  the  animal. 

§  52.  Differential  Diagnosis.  The  diagnosis  is  made 
by  finding  the  .streptococcus  in  pure  culture.  It  is  to  be  dif- 
ferentiated from  the  sporadic  cases  of  mastitis  caused  primarily 
by  some  injury,  and  the  infectious  mastitis  caused  by  other 
bacteria,  largely  micrococci.  This  can  readily  be  done  from  a 
bacteriological  examination  of  the  udder  secretions. 

§  53.  Prevention.  This  disease  is  spread  from  the 
infected    to    the    non-infected    largely    by    the    hands   of  the 


62  STREPTOCOCCUS    MASTITIS 

milkers.  Recognizing  this  fact,  the  spread  can  be  stopped 
by  disinfecting  (washing  in  a  disinfectant)  the  hands  of  the 
milker  after  each  animal.  The  diseased  animals  should  be 
isolated  from  the  others.  It  is  one  of  the  easiest  infections 
to  control. 

REFERENCES. 

1.  Brennwald.  Chronische  Euteretitziindung,  Archivf.  Thier- 
heilk.     Bd.  X  (1848),  S.  40. 

2.  Dubois.  An  Enzooty  of  Acute  Streptococcic  Mammitis.  Jour. 
Contp.  Path,  and  Thera.     Vol.  XVII  {1894),  p.  159. 

3.  NoCARD  ET  MoLi-ERE.\u.  Sur  une  mammite  contagieuse  des 
vaches  laitieres.  Bulletin  de  la  Societe  centr.  de  Med.  vet.,  1884,  p.  188. 
Ibid.     Ann.  de  PJnstiiut  Pasteur,  Vol.  I  (1887),  p.  109. 

4.  Reed  and  Ward.  The  significance  of  the  presence  of  strepto- 
cocci in  market  milk.     American  Medicine,  Vol.  VII  (1903),  p.  256. 

5.  ZSCHOKKE.  Weitere  Untersuchungen  iiber  den  gelben  Gait. 
Schweizer-Archiv  fi(r  Thierheilk.,  Bd.  XXXIX  (1897),  S.  145. 


CHAPTER  IV. 


DISEASES  CAUSED  BY  BACTERIA 
GENUS  MICROCOCCUS. 


§  54.     General  discussion  of  the  genus  Micrococcus. 

^h.Q: genus  Micrococcus  includes  the  spherical  bacteria  that  divide 
in  two  planes.  The  micrococci,  therefore,  may  be  single  spher- 
ical organisms  or  they  may  be  united  in  pairs  (diplococcus), 
in  fours  (tetracoccus),  or  in  small  clumps  or  masses  (staphy- 
lococcus). This  genus  contains  many  important  species  but 
they  are  largely  among  those  forms  producing  wound  infection, 
such  as  Micrococcus  pyogenes  aureus.  These  infections  are  not 
characteristic  in  their  manifestations  and  consequently  the 
disturbances  they  produce  have  not  been  classed  among  the 
specific  infectious  diseases.  At  present,  we  seem  to  have 
recognized  but  one  specific  malady  of  animals  attributed  to 
them.     In  the  human  species  they  cause  a  number  of  diseases. 


TAKOSIS. 


§  55.  Characterization,  Takosis,  meaning  to  waste,  is 
a  destructive,  infectious  disease  of  angora  goats.  It  is  char- 
acterized by  great  emaciation  and  weakness,  with  symptoms 
of  diarrhea  and  pneumonia. 

§  56.  History.  The  name  Takosis  was  given  to  this 
disease  of  goats  by  Mohler  and  Washburn  in  1903.  They  in- 
vestigated the  disease,  described  its  symptoms  and  morbid 
anatomy.  They  found  a  micrococcus  which  they  believed  to 
be  its  cause  and  which  they  named  M.  caprimis. 

In  1875,  a  disease  was  reported  among  angora  goats  in 
Virginia  which  may  have  been  this  infection.  Pegler  describes 
it  somewhat  fully  in  his  work  entitled,  ' '  The  book  of  the  goat ' ' 


THh 

R31TY  i 


64  TAKOSIS 

as  "  a  disease  peculiar  to  goats."  The  identity  of  this  disease 
and  the  various  affections  of  goats,  largel}'  pneumonia, 
described  bj^  Duquesnoy,  Hutchens,  Pusch,  Steele  and  others 
is  not  established.  Mohler  and  Washburn  seem  to  be  the  only 
investigators  in  this  country  who  have  carefully  studied  this 
affection. 

§  57.  Geographical  Distribution.  Takosis  is  reported 
from  a  number  of  localities  in  this  country,  more  especially  in 
the  Northern  States. 

§  58.  Etiology.  Accord- 
ing to  Mohler  and  Washburn 
this  disease  is  caused  by  M. 
caprinus.  It  is  pathogenic 
for  goats,  chickens,  rabbits, 
guinea  pigs  and  white  mice, 
but  not  for  sheep,  dogs  or 
rats.  It  usually  appears  in 
pairs.  It  has  been  isolated 
in  pure  culture  from  the 
heart's  blood, spleen,  kidneys 

and    pericardial    fluid.        It       ^      ,,      ...  ^    . 

^  Fig.  8.     Micrococcus  caprinus Jrom 

was  not  obtained  in  cultures   ^/^^    ^^^^^^^    ,,y-    ^„     ^„„.^^^,     ^^^^ 

from  the  spinal  cord.  {Mohler). 

^5  59.  Symptoms.  The  first  observable  symptom  is  a 
listless  and  languid  appearance  of  the  animal.  The  affected 
goats  lag  behind  the  flock.  Frequently  there  is  drooping  of 
the  ears  and  a  drowsy  appearance  of  the  eyes.  There  is  slight 
elevation  of  the  temperature  in  the  beginning,  but  later  in  the 
course  of  the  disease  it  becomes  subnormal.  As  the  disease 
advances  the  goats  move  about  in  a  desultory  manner,  the 
back  arched,  neck  drawn  down  toward  the  sternum,  and  the 
gait  staggeriug.  Rumination  is  seldom  impaired.  The  appe- 
tite is  usually  good  but  capricious.  The  exposed  mucous 
membranes  are  pale.  The  respirations  are  accelerated  and 
labored.  The  affected  animals  soon  become  so  weak  that  they 
can  stand  with  difficulty,  and  often  they  are  knocked  down 


MORBID    ANATOMY  65 

and  trampled  by  their  companions.  They  shrink  often  to 
nearly  half  their  normal  weight.  There  is  usually  a  fluid  dis- 
charge from  the  bowels  of  a  very  offensive  odor  during  the 
last  few  days.  The  goat  groans  occasionally  and  the  head  is 
usually  bent  around  to  one  side.  Death  follows  in  from  eight 
days  to  ten  weeks.  Recoveries  have  not  been  observed.  The 
young  are  reported  to  be  more  susceptible  to  the  disea.se  than 
the  older  animals. 

§  60.  Morbid  anatomy.  Emaciation  and  anemia  are 
the  most  striking  lesions.  The  lungs  usually  contain  areas  of 
pneumonia.  Their  surface  is  mottled  by  areas  of  congestion 
and  iron  gray  patches.  On  section  these  areas  show  a  frothy 
mucus  in  the  bronchioles.  The  heart  mu.scle  is  pale,  dull,  soft 
and  flabby.  Inflamed  hemorrhagic  areas  may  appear  on  the 
epicardium.  Sometimes  they  are  present  in  the  endocardium 
especially  that  lining  the  ventricles.  The  pericardium  is 
slightly  thickened  and  usually  contains  a  small  quantity  of 
blood-stained  fluid.  The  gall  bladder  is  frequently  distended 
with  a  pale-yellow  watery  bile.  The  liver  appears  to  be  unaf- 
fected. The  kidneys  are  anemic  and  softened.  The  cortex  is 
pale  and  contrasts  strongly  with  the  dark  pyramids.  The 
capsule  is  easily  removed.  The  spleen  appears  to  be  atrophied 
and  indurated,  the  fibrous  portions  exceeding  the  spleen  pulp. 
The  spleen  may  be  attached  to  the  diaphragm  or  neighboring 
organs  by  adhesions.  The  mucosa  of  the  intestines  gives  the 
appearance  of  a  chronic  catarrh  associated  with  necrosis  of  the 
mucosa. 

The  microscopic  study  showed  the  terminal  bronchioles 
and  alveolar  passages  to  have  swollen  walls  and  to  contain 
various  amounts  of  mucus  and  desquamated  cells  as  a  result 
ot  the  catarrhal  inflammation.  The  blood  vessels  in  the  inter- 
alveolar  tissue  are  distended  and  surrounded  by  migrated 
leucocytes.  The  kidneys  show  a  catarrhal  or  parenchymatous 
nephritis  with  the  most  pronounced  changes  occurring  in  the 
cortex.  The  intercapsular  space  is  dilated  and  contains  an 
albuminous  exudate.  The  convoluted  tubules  show  the  epi- 
thelium to  be  swollen  and  granular  and  occasionally   desqua- 


66  TAKOSIS 

mated.  The  tubules  may  contain  an  albuminous  deposit.  As 
the  specific  micrococcus  has  not  been  found  in  the  kidneys, 
Mohler  and  Washburn  considered  the  lesions  in  this  organ  to 
be  of  toxic  origin. 

The  heart  shows  parenchymatous  degeneration  of  isolated 
fibers  or  groups  of  fibers.  The  spleen  shows  an  increase  in 
fibrous  tissue.  Sections  of  the  intestines,  especially  of  the 
duodenum,  show  a  productive  inflammation  with  exudation. 
There  is  often  desquamation  of  the  mucosa. 

The  blood  count  in  experimental  cases  shows  an  increase 
in  the  number  of  red  corpuscles.  Mohler  and  Washburn  report 
the  examination  of  the  blood  in  two  such  cases  and  one  of  nat- 
ural infection  as  follows  : 

No.  I.  Red  corpuscles  11,190,000,  white  corpuscles  20,560 
per  cubic  millimeter. 

No.  2.  Red  corpuscles  12, 160,000,  white  corpuscles  20,000 
per  cubic  millimeter. 

No.  3.  (Natural  infection)  red  corpuscles  10,208,000, 
white  corpuscles  14,860  per  cubic  millimeter. 

They  give  the  normal  red  corpuscles  as  9,976,000,  white 
corpuscles  9,200  per  cubic  millimeter. 

The  increase  in  the  white  cells  they  state  is  due  to  an  in- 
creased number  of  polymorphonuclear  leucocytes  and  eosin- 
ophils. They  found  the  specific  "gravity  of  the  blood  to  be 
1. 03 1  and  hemoglobin  56. 

§  61.  Differential  Diagnosis.  Takosis  is  to  be  differen- 
tiated from  the  morbid  condition  resulting  from  various  animal 
parasites,  anemia  caused  by  some  previously  existing  disease 
such  as  chronic  pneumonia,  or  poor  food  and  starvation  ; 
watery  cachexia  and  hydremia,  and  contagious  pneumonia. 

The  positive  diagnosis  is  made  from  the  infectious  nature 
of  takosis,  and  by  finding  the  specific  organism,  M.  caprinus 
in  the  tissues.  The  symptoms  caused  by  parasites -frequently 
resemble  quite  closely  those  of  takosis.  In  takosis  symptoms 
of  pneumonia  will  frequently  be  noted,  especially  the  labored 
breathing  or  rapid  respiration.     The  luster  of  the  fleece  is  less 


PREVENTION  07 

affected  in  takosis,  while  diarrhea  is  more  frequently  noted. 
Continuous  coughing  and  snuffling,  while  diagnostic  of  the 
presence  of  lung  worms,  are  not  characteristic  of  takosis. 

The  anemia  due  to  other  causes  is  not  common.  Hy- 
dremia usually  results  from  poor  feeding  or  pasturing  on  low 
ground.  The  symptoms  are  weakness,  exhaustion,  rapid 
respiration  and  palpitating  heart.  The  mucosa  of  the  eyes, 
nose  and  mouth  are  pale  and  swollen.  The  edema  about  the 
head,  neck  and  abdomen  will  differentiate  this  condition  from 
takosis. 

Hutcheou  writes  concerning  the  contagious  pneumonia  of 
goats  as  follows  : 

"  It  was  a  specific  infectious  form  of  pleuro-pneumonia, 
affecting  goats  only.  Cattle  and  sheep  remaining  free  from 
infection  although  constantly  exposed  to  it.  The  disease  was 
introduced  into  Cape  Colony  by  a  shipload  of  angora  goats 
from  Asia  Minor,  where  the  disease  is  represented  as  being 
indigenous." 

§62.  Prevention.  The  study  of  this  disease  by  Mohler 
and  Washburn  brought  out  very  clearly  certain  preventive 
measures  that  should  be  carefully  noted. 

1.  The  most  destructive  outbreaks  have  occurred  among 
goats  that  had  recently  been  shipped  from  a  Southern  locality 
to  a  Northern  latitude.  Sudden  climatic  changes  should  be 
avoided.  Hob.son  states  that  the  natives  of  Asia  Minor  assert 
that  the  goat  cannot  be  transported  from  one  village  to  another 
of  higher  altitude  without  suffering  some  deterioration. 

2.  Angora  goats  should  be  provided  with  stables  that 
are  perfectly  dry.  These  should  be  accessible  to  them  at  all 
times,  as  rains  are  very  injurious  to  them.  So  averse  are  they 
to  wetting  that  they  will  seldom  be  caught  out  in  a  shower  if 
shelter  is  within  reach. 

3.  Careful  feeding. 

4.  When  the  disease  appears,  remove  all  well  animals 
from  the  sick  ones. 

Immunity  seems  to  have  been  established  by  the  injection 


68  TAKOSIS 

subcutaneously  of  sterilized  cultures  of  the  specific  organism. 
The  method,  however,  is  still  in  the  experimental  stage. 

REFERENCES. 

1.  HOBSON.  Angora  goat  farming.  Agricultural  Journal,  Cape 
Colony,  Vol.  VIII  (1894),  p.  81. 

2.  H01.ZENDORFF.  Lungen-Brustfellentziindung  bei  Ziegen. 
Archivfiir  Thierheilk.,  Bd.  XXII  (1896),  p.  345. 

3.  HuTCHEON.  Contagious  pleuro-pneumonia  in  Angora  goats. 
The  Veterinary  Journal,  Vol.  XIII  (1881),  p.  171. 

4.  HuTCHEON.  Contagious  pleuro-pneumonia  in  goats  at  Cape 
Colony,  South  Africa.     Ibid.  Vol.  XXIX  (1889),  p.  399. 

5.  MoHLER  and  Washburn.  Takosis,  a  contagious  disease  of 
goats.  Bulletin  No.  45,  U.  S.  Bureau  of  Animal  Industry,  Washing- 
ton, D.  C,  1903. 

6.  NicoL  ET  Refik-Bey.  La  pneumonic  des  chevres  d'Anatolie. 
Ann.  de  Vhist.  Pasteur,  Vol.  X  (1886),  p.  321. 

7.  Pegler.     The  book  of  the  goat.     1885. 


CHAPTER  V. 

DISEASES  CAUSED  BY  BACTERIA 
GENUS  BACTERIUM. 


§  63.  General  discussion  of  the  genus  bacterium. 
The  genus  Bacterium  includes  all  the  rod-shaped,  non-motile 
bacteria.  The  absence  of  raotihty  appears  to  be  a  logical, 
natural  and  sufficient  reason  to  place  these  organisms  in  a 
genus  by  themselves.  The  only  objection,  that  can  be  reason- 
ably urged  against  it  from  the  pathologist's  point  of  view,  is 
the  changing  of  the  generic  name  of  a  number  of  important 
pathogenic  bacteria,  such  as  those  of  anthrax,  glanders,  tuber- 
culosis and  others,  from  Bacillus  to  Bacterium/>  This,  how- 
ever, is  not  serious  but  should  be  gladly  welcomed  if  it  enables 
us  to  bring  into  groups  for  study  diseases  that  are  etiologically 
more  closely  related.  It  is  for  this  reason  that  the  classifica- 
tion is  adopted.  The  further  subdivision  of  the  non- motile, 
rod-shaped  bacteria  into  several  genera,  as  found  in  more 
recent  classifications,  suggests  the  possible  desirability  of  a 
more  restricted  grouping  of  diseases  for  study  and  comparison, 
than  Migula's  classification  permits.  Several  writers  have 
already  proposed  a  more  limited  grouping,  such  as  is  found  in 
the  Pasteur  el  loses. 

^  64.  Pasteurelloses.  Lignieresv  has  introduced  the 
term  Pasteurelloses  to  include  a  group  of  diseases  in  different 
species  of  animals  caused   by  the  bacteria  represented  by  the 

*  It  is  important  not  to  confuse  the  genus  bacterium  as  revived  by 
Migula  with  the  same  genus  of  earlier  writers  who  characterized  it  as 
composed  of  non-spore  bearing,  rod-shaped  organisms. 

T  Lignieres.  Contribution  a  I'etude  et  a  la  classification  des  septi- 
cemics hemorrhagiques  les  "  Pasteurelloses."  Ami.  de  Vlnstit.  Pasteur, 
Vol.  XV  (1901),  p.  734- 


70 


PASTEURELLOSES 


bacterium  of  fowl  cholera,  first  described  by  Pasteur.  Trevisan 
gave  the  generic  name  Pasteiirella  to  this  group  of  organisms. 
Hueppe  designated  them  under  the  heading  of  Bacillus  septi- 
cetniac  hemorrhagicac.  He  seems  to  have  taken  for  his  type 
the  bacillus  of  schweineseuche  of  Loeffler  and  Schiitz. 

In  order  to  simplify  the  nomenclature,  Lignieres  has 
grouped  the  diseases  caused  by  the  Pastcurella  Trev.  as  indi- 
cated below.  This  plan  was  adopted  by  Nocard  and  Leclainche. 

1.  Pastenrellose  of  birds.      Fowl  cholera. 

2.  Pastenrellose  of  rabbits.      Rabbit  septicemia. 

3.  Pasteurello.se  of  guinea-pigs. 

4.  Pasteurellose  of  wild  animals.      Wildseuche. 

5.  Pasteurellose  of  sheep.     Pneumo-enteritis  of  sheep. 

6.  Pasteurellose  of  goats.     Infectious  pneumonia. 

7.  Pasteurellose  of  cattle.       Septicemia     hemorrhagica, 

septic  pleuro-pneumonia  of  calves, 
diarrhea  of  calves  (white  scours)  and 
enteque  ( a  disease  of  cattle  in  Argen- 
tine Republic,  characterized  by  a  state 
of  progressive  cachexia. ) 

8.  Pasteurellose  of  buffalo.      Barbone,  an  infectious  dis- 

ease of  buffalo  characterized  by  acute 
fever  and  edematous  engorgement  of 
various  organs. 

9.  Pasteurellose  of  swine.     Swine  plague. 

10.  Pasteurellose  of  horses.       Infectious    pneumonia    or 

typhoid  fever  of  horses. 

11.  Pasteurellose  of  dogs.   Maladie  des  chiefis  {(Msiem^&r) 

and  typhus  du  chien  (malady  of  Stutt- 
gart, hemorrhagic  gastro-enteritis. ) 
The  very  interesting  and  far  reaching  findings  of  Lig- 
nieres relative  to  the  distribution  of  this  genus  of  bacteria  and 
the  diseases  produced  by  its  different  species  are  worthy  of 
careful  consideration.  If  his  results  are  verified,  this  grouping 
will  do  much  to  simplify  both  the  nomenclature  and  the  de- 


SWINE    PLAGUE  71 

scriptions  of  the  various  maladies  caused  by  this  group  of  bac- 
teria. We  already  have  a  similar  grouping  in  tuberculosis, 
where  the  disease  bears  the  name  of  its  cause,  no  matter  in 
what  species  of  animals  it  exists  or  in  what  form  it  manifests 
itself.  Such  a  simplying  process  is  hoped  for  but  at  present 
it  seems  desirable  to  retain  the  names  of  the  diseases  that  are 
now  recognized. 


SWINE  PLAGI'R* 

Sy>nniy»is.  Infectious  pneumo-enteritis.  Pasteurellose 
of  swine  ;  sepficeuiic  du pore :  p)ieumonii  contagieuse ;  Schwein- 
cseiuhe. 

>^  65.  Characterization.  Swine  plague  is  an  infectious 
disease  of  swine  occurring  sporadically  and  in  epizootics.  It 
appears  usually  as  a  septicemia,  or  a  pneumonia  in  which  there 
is  marked  consolidation  of  the  ventral  and  cephalic  lobes  and 
the  cephalic  portion  of  the  principal  lobe  of  one  or  both  lungs. 
There  may  or  may  not  be  pleuritis.  There  may  be  marked 
changes  in  the  intestine,  consisting  of  superficial  necrosis  of 
the  mucosa  especially  in  the  ileum  and  cecum.  On  this 
account  it  has  been  considered  an   infectious  pneumo-enteritis. 

§  66.  History.  In  1886,  Smith  found  in  a  pig  in  the 
state  of  Illinois  a  disease  which  differed  from  hog  cholera,  and 
from  the  lesions  he  isolated  an  organism  which  differed  from 
the  bacillus  of  hog  cholera.  Later  other  cases  of  thisdisea.se 
were  found  in  considerable  numbers  not  only  in  the  state  of 
Illinois  but  in  various  places  in  the  eastern  part  of  the  United 
States.  Prior  to  this,  Loeffler  in  Germany  had  described  an 
organism  which  he  had  found  to  be  the  cause  of  an  infectious 
pneumonia  in  swine  {Schiveinesciiche )  and  with  which  Smith 
was  able  to  identify  the  organism  he  had  discovered.  The  first 
publication    on    this    disease    in   the  United   States  is   in    the 

*  For  an    explanation    of   the   confusion   existing   concerning;   llie 
nomenclature  of  swine  plague  and  hog  cholera  see  hog  cholera. 


72 


SWINE  PLAGUE 


Annual  Report  of  the  Bureau  of  Animal  Industry  for  1886. 
Smith  described  swine  plague  as  an  independent  disease, 
although  it  is  often  associated  with  hog  cholera  in  the  same 
animal.  On  account  of  its  frequent  association  with  hog 
cholera,  it  has  been  thought  by  some  investigators  to  be  a 
secondary  infection  only.  In  1895  the  writer  investigated 
several  outbreaks  of  this  disease  in  southern  Minnesota  where 
it  occurred  uncomplicated  with  hog  cholera.  More  recently 
two  epizootics  of  swine  plague  have  been  studied  in  New  York 
State  where  no  evidence  was  found  of  its  being  a  secondary 
infection  but  where  in  every  particular  its  independent  nature 
was  indicated. 


^  67.  Geographical  distribution.  Swine  plague  is  a 
wide  spread  disease  in  this  country.  It  seems  to  occur  more 
or  less  frequently  in  every  state  in    the   Union.      It    is    quite 

widely  distributed  in  Ger- 
many, but  to  what  extent  it 
exists  in  other  countries 
there  is  little  or  no  available 
evidence. 

^  68.  Etiology.  Swine 
plague  is  caused  by  a  non- 
motile,  elongated,  oval  bac- 
terium described  by  Smith  in 
1886.  It  is  identical  with 
the  bacillus  of  Schzveineseuche 
decribed  by  Loeffler  in  1885. 
Fig.  9.  Bacterium  of  swine  plague  Hueppe  proposed  the  name 
from  a  cover-glass  preparation  of  a  Bacterium  septicemiae  hemor- 
rabbiVs  liver.  rhagicae  for  this  organism. 

Hutyra  has  found  a  filterable  virus  in  the  blood  and  other 
parts  of  pigs  suffering  with  Schiveincseuche.  The  possibility 
of  a  mixed  infection  in  this  case  is  not  excluded.  Other 
European  observers  have  reported  similar  findings. 

The  bacterium  of  swine  plague  and  its  varieties  have  not 
been    systematically    studied   and    classified.     It   has   already 


ETIOLOGY 


73 


been  noted  that  the  bacteria  of  rabbit  septicemia,  fowl  cholera 
and  Wildseuche  are  closely  related  to  it. 

Becker  has  described  a  pleuro-pneumonia  in  lambs  and 
Evans  has  recently  observed  a  septicemia  hemorrhagica  in 
elephants  caused  by  this  species  of  bacteria.  The  infection 
took  place  through  wounds. 

The  pathogenic  organism  associated  with  the  lesions  in 
certain  forms  of  broncho-pneumonia  in  cattle  diflfers  very 
slightly  from  this.  In  human  pathology,  we  find  a  striking 
resemblance  in  Micrococcus  lanccolahis  to  the  swine-plague  bac- 
terium, especially  in  its  manifold  and  varied  pathogenic  possi- 
bilities and  its  frequent  presence  in  normal  saliva. 

The  fact  should  be  recognized  that  experimentally  the 
different  varities  or  forms  of  this  group  {Bacterium  septi- 
cemiae  hemorragicae  HxiQ-p^t,  Paste urella  Trev.)arenot  inter- 
changeable in  their  pathogenesis  except  for  the  rabbit.  Thus 
an  epizootic  form  of  fowl  cholera  has  not  been  produced  with 
the  swine  plague  or  rabbit  septicemia  organism.  Further,  it 
has  been  shown  that  in  the  upper  air  passages  of  healthy 
swine,  cattle,  horses,  cats  and  dogs*  there  are  bacteria  not 
distinguishable  in  their  cultural  characters  and  their  effect 
upon  rabbits  from  the  swine  plague  bacterium.  The  presence 
of  this  organism  in  the  trachea  of  healthy  pigs  has  been  sug- 
gested as  the  source  of  the  cause  of  sporadic  cases  of  swine- 
plague.  It  explains  the  frequent  association  of  this  bacterium 
with  hog  cholera  and  other  maladies.  What  the  conditions 
are  by  which  this  organism  is  enabled  to  produce  disease  in  its 
host  have  not  been  clearly  pointed  out. 

If  the  rabbit  is  taken  as  the  animal  on  which  to  test  the 
pathogenesis  of  the  bacteria  belonging  to  the  swine  plague 
group,  we  find  that  those  from  different  sources  are  very  simi- 
lar. In  nature,  the  bacteria  of  swine  plague,  rabbit  septi- 
cemia, fowl  cholera,  and  those  located  in  the  normal  upper  air 
passages  of  the  various  species  of  animals  mentioned  exist, 

*The  investigations  thus  far  made  show  these  bacteria  to  be  present 
in  48  per  cent  of  healthy  swine,  80  per  cent  of  cattle,  50  per  cent  of 
sheep,  16  per  cent  of  horses,  90  per  cent  of  cats,  and  30  per  cent  of  dogs. 


74  SWINE    PLAGUE 

possessed  of  marked  variation  in  virulence,  that  is,  there  are 
those  that  will  kill  a  rabbit  in  from  1 6  to  24  hours  when  inoc- 
ulated subcutaneously  with  a  pure  culture  and  those  that 
require  from  3  to  10  days,  or  even  weeks,  to  destroy  life. 
With  the  variations  in  the  time  period,  we  have  corresponding 
differences  in  lesions.  The  virulent  forms  produce  septicemia 
while  the  attenuated  varieties  excite  a  severe  purulent  infiltra- 
tion about  the  place  of  inoculation  and  exudates  on  one  or 
more  of  the  serous  membranes.  Conversely,  it  has  been  shown 
that  rabbits  possessed  of  a  certain  amount  of  natural  or  artifi- 
cially produced  resistance  will,  when  inoculated  with  a  viru- 
lent culture,  die  after  the  same  period  of  time  and  with  lesions 
similar  to  those  produced  by  the  attenuated  virus  in  the  sus- 
ceptible rabbit. 

■  The  fact  that  this  organism  is  not  frequently  described  in 
our  works  on  bacteriology  and  because  of  some  confusion 
existing  concerning  it  and  the  bacillus  of  hog  cholera,  it  is 
deemed  best  to  insert  a  short  description  of  it  here. 

^  6g.  Brief  description  of  the  bacterium  of  swine 
plague. 

Morphology. — A  non-motile,  rod-shaped  organism  varying  from  o.S 
to  2.0  microns  in  length  and  from  0.4  to  1.2  microns  in  breadth.  The 
ends  are  oval,  and  the  shorter  forms  resemble  micrococci.  The  size 
depends  upon  the  medium  and  the  stage  of  development  of  the  individ- 
ual bacteria.  A  capsule  has  not  been  demonstrated,  although  often 
there  appears  to  be  one  in  preparations  made  directly  from  tissues.  It  is 
not  observed  in  cultures.  Spores  have  not  been  seen.  Involution  forms 
are  not  uncommon  in  old  cultures.  They  are  especially  numerous  in 
the  organs  of  a  rabbit  when  it  is  allowed  to  lie  for  some  hours  after 
death  before  it  is  examined.  It  exhibits,  when  stained  in  cover-glass 
preparations  made  directly  from  animal  tissues,  a  light  center  with 
deeply  stained  extremities  (polar  stain  i.  In  preparations  made  directly 
from  cultures  this  character  is  much  less  marked.  It  stains  readily  with, 
the  basic  aniline  dyes.  It  does  not  retain  the  coloring  matter  when 
stained  after  Gram's  method. 

Cultural  and  biochemic  properties. — This  organism  is  less  hardy 
than  the  bacillus  of  hog  cholera,  and  on  certain  of  the  media  used  it 
grows  very  feebly  or  not  at  all.  It  requires  a  temperature  of  above  37° 
C.  although  it  develops  very  slowly  at  the  room  temperature. 


15ACTKRIUM  75 

Agar. — The  growth  on  this  medium  is  not  vigorous.  It  is  of  a 
neutral  grayish  color,  with  a  glistening,  moist  appearing  surface.  It  is 
slightly  viscid  and  adheres  to  the  agar  surface.  Isolated  colonies  vary 
from  I  to  2  mm.  in  diameter,  nearly  round,  convex,  with  smooth  and 
sharply-defined  margins.  The  condensation  water  becomes  faintly 
clouded  with  a  grayish  sediment  which  becomes  viscid.  Within  the 
agar  the  colonies  appear  as  minute  grayish  dots.  In  agar,  especially  in 
plates  (Petri  dishes),  it  emits  a  peculiar,  disagreeable,  pungent  odor. 

Gelatin. — Ordinarily  it  does  not  grow  in  gelatin.  (Dr.  Theobald 
Smith  found  that  certain  cultures  grew  in  this  medium.) 

Potato.— \i  does  not  grow  on  potato. 

Bouillon. — Alkaline,  peptonized  bouillon  becomes  uniformly 
cloxided  in  24  hours  when  kept  at  a  temperature  of  36°  C.  Occasionally 
cultures  are  obtained  in  which  the  growth  appears  in  the  form  of  floc- 
culent  masses,  but  usually  after  a  few  generations  these  disappear  and 
the  liquid  becomes  uniformly  cloudy.  If  the  bouillon  contains  any 
dextrose  or  muscle  sugar,  its  reaction  becomes  acid  in  24  to  48  hours, 
owing  to  the  fermentation  of  the  carbohydrate.  With  the  virulent  cul- 
tures the  liquid  clears  within  a  few  days.  The  small  amount  of  grayish 
sediment  becomes  viscid  after  some  days,  and  upon  agitation  it  is 
forced  up,  appearing  as  a  somewhat  twisted,  tenacious  cone,  with  its 
apex  at  or  near  the  surface  of  the  liquid.  Frequently  a  thin,  grayish, 
somewhat  viscid  band  composed  of  bacteria  is  found  on  the  sides  of  the 
tube  at  the  surface  of  the  liquid.  It  will  not  grow  in  acid  bouillon.  If 
the  bouillon  contains  from  i  to  2  per  cent,  glucose,  the  growth  is 
slightly  more  vigorous. 

Effects  on  sugars.  — lnih.Qiexmenta.i\on  tube,  alkaline  bouillon  con- 
taining sugars  becomes  uniformly  clouded  in  both  branches,  tras  is 
not  produced.  In  bouillon  containing  dextrose  and  saccharose  the 
reaction  becomes  strongly  acid  in  24  hours,  but  the  reaction  of  alkaline 
bouillon  containing  lactose  is  not  changed. 

7I/i7/&.— Milk  inoculated  with  this  organism  remains  unchanged  in 
appearance  for  several  weeks.  When  boiled,  after  this  period,  the 
casein  is  not  coagulated. 

Indol. — This  organism  grows  feebly  in  Dunham's  solution;  some 
cultures  have  given  a  decided  indol  reaction,  but  others  have  not.  The 
production  of  indol  is  reported  to  be  one  of  the  properties  of  the  German 
swine  plague.  Smith*  obtained  only  a  trace  of  indol  in  one  out  of  four 
cultures  of  swine-plague  bacteria. 

/%,?«(7/.— This  was  found  bv  Lewandowski'st  method   in   all  of  the 


*Special  report  on  swine  plague,  1891,  p.  89. 
tDeutsche  med.  Wochenschrift,  1890,  S.  iiSb. 


76  SWINE    PLAGUE 

cultures  tested  by  Smith.  I  have  failed  to  obtain  the  reaction  in  a  few 
cultures,  but  usually  it  appears. 

Thermal  death  point. — This  organism  is  destroyed  in  bouillon  at 
58°  C.  in  ten  minutes.  A  temperature  of  56°  C.  for  this  time  did  not 
destroy  its  vitality. 

Effect  0/ drying. — These  bacteria  cannot  stand  drying.  The  bacte- 
ria in  a  drop  of  bouillon  dried  on  a  cover-glass  and  kept  at  the  room 
temperature  are  destroyed  in  24  to  36  hours.  In  similar  preparations 
made  from  agar  cultures  they  resist  drying  from  five  to  eight  days. 
The  difference  in  the  time  between  the  two  cultures  is  probably  due  to 
the  thicker  layer  in  case  of  the  agar  preparations. 

Persistence  of  vitality  in  icater  and  .yo//.— Experiments  to  deter- 
mine the  length  of  time  this  organism  will  live  in  water  and  in  the  soil 
show  that  it  is  destroyed  in  water  in  test  tubes  in  from  nine  to  eleven 
days.  In  the  soil  it  was  not  found  after  eight  days.  Dr.  Smith  states 
that  it  is  destroyed  in  the  soil  after  four  days. 

PoK'er  to  resist  disinfectants. — The  bacterium  of  swine  plague  is 
very  sensitive  to  the  action  of  disinfectants.  A  large  number  of  these 
agents  have  been  tested.     The  following  are  among  the  more  important  : 

Commercial  sulphuric  acid,  "s  per  cent,  kills  in  30  minutes. 

Commercial  hydrochloric  acid,  %  per  cent,  kills  in  10  minutes 

L/ime,  lime  water  kills  in  i  minute. 

Lime,  0.015  per  cent,  kills  in  30  minutes. 

Carbolic  acid,  '4  per  cent,  kills  in  60  minutes. 

Carbolic  acid,  i  per  cent,  kills  in  5  minutes. 

Carbolic  acid,  2  per  cent,  kills  in  i  minute. 

Formalin,  solution  1:2000  kills  in  5  minutes. 

Trikresol,  ;/,  per  cent,  kills  in  5  minutes. 

Pathogenesis. — This  organism  is  pathogenic  for  rabbits,  guinea  pigs 
and  mice  amongthe  smaller  experimental  animals  and  for  swine.  With 
the  virulent  form  rabbits  inoculated  either  subcutaneously  or  in  the 
vein  with  very  small,  o.ooi  c.  c.  doses,  die  of  septicemia  in  from  16  to  24 
hours.  Guinea  pigs  are  slightly  less  susceptible.  When  inoculated 
subcutaneously  with  o.  I  to  0.2  c.  c.  of  a  bouillon  culture,  they  die  in 
from  30  to  72  hours.  Mice  succumb  in  about  24  hours  when  inoculated 
with  a  drop  of  the  culture.  Pigs  inoculated  intravenously  usually  die 
from  acute  septicemia  in  from  18  to  36  hours.  If  they  live  longer  there 
may  be  decided  lung  lesions.      (See  report  on  swine  plague.  Smith  ) 

§  70.  Symptoms.  It  is  frequently  difficult  to  recognize 
symptoms  distinctive  of  swine  plague.  The  peculiarities  of 
swine  render  it  exceedingly  difficult  to  obtain  evidence  on 
physical  examination  of  lung  disease.     Sometimes  this  affec- 


MOKKID    ANATOMY 


77 


tion  runs  a  very  rapid  course,  the  animal  dying  of  septicemia. 
Usually  it  is  more  protracted,  lasting  from  a  few  days  to  a 
week  or  longer.  Animals  affected  with  the  more  chronic  form, 
where  there  are  lung  lesions,  eat  very  little  or  refu.se  food 
altogether.  They  cough  considerably,  especially  when  forced 
to  run.  The  back  is  usually  arched  and  the  groins  sunken. 
The  whites  of  the  eyes  are  reddened.  The  skin  over  the 
ventral  surface  of  the  body,  nose  and  ears  is  frequently  flushed. 
The  cough,  however,  is  the  most  reliable  indication  we  have 
of  swine  plague  ;  but  in  some  cases  of  hog  cholera  the  coexist- 
ence of  broncho-pneumonia  also  causes  the  animal  to  cough 
when  forced  to  move  rapidly. 

§  71.  Morbid  anatomy.  There  are  many  known  varia- 
tions in  the  appearance  of  the  internal  organs  of  hogs  which 
have  died  of  swine  plague.  The  characteristic  lesions  are.  as 
previously  stated,  to  be  found  in  the  lungs.  Frequently  the 
abdominal  viscera  appear  to  be  normal,  although  a  careful 
examination  will  usually  reveal  slight  changes.  In  the  lungs, 
however,  the  disease  is  ordinarily  obvious. 

The  variety  of  lesions  produced  by  the  inoculation  of 
swine  plague  bacteria  is  not  so  great  as  that  observed  in  the 
naturally  contracted  disease.  While  there  are  outbreaks  in 
which  considerable  uniformity  is  observed,  there  are  others  in 
which  each  animal  is  a  surprise  to  the  pathologist.  In  general 
it  may  be  stated  that  the  lungs  and  the  digestive  tract  are  the 
chief  seats  of  the  disease,  though  other  organs,  notably  the 
lymphatic  glands,  are  secondarily  involved.  The  disease  is 
localized  in  the  lungs  and  in  the  digestive  tract  probably 
because  the  bacteria  gain  entrance  through  the  respiratory  and 
digestive  passages. 

The  lungs  have  been  found  diseased  in  nearly  every  out- 
break which  has  been  investigated.  In  some  outbreaks  the 
lung  lesions  predominated  and  pneumonia  was  the  direct  cause 
of  death.  In  individual  cases,  pneumonia  is  absent  but 
pleuritis  and  interlobular  edema  are  generally  present.  In  a 
few  instances  interlobular  emphysema  of  the  lungs  has  been 
observed.      With   pneumonia  the  seat    of  the    le.sion    varies  : 


78 


SWINE    PLAGUE 


usually  the  ventral  lobes  are  first  attacked,  then  the  cephalic 
and  azyffos,  and  lastly  the  principal  lobes.  This  movement  of 
the  disease  seems  to  depend  on  gravity,  inasmuch  as  the  dis- 
eased parts  are  marked  off  from  the  healthy  portion  by  a  nearly 

horizontal  line.  I  n 
other  words,  the  most 
dependent  portions  of 
the  lungs  are  the  ones 
affected  first,  and  as 
the  disease  progresses 
upwards  only  a  small 
portion  of  the  princi- 
pal lobe  directly  un- 
der the  back  of  the 
animal  remains  per- 
vious, provided  the 
life  of  the  animal  is 
maintained  up  to  this 
point.  In  cases  where 
disease  is  caused  by 
lung  worms  or  by  em- 
bolism, the  pneu- 
monia involves  por- 
tions of  the  principal  lobes  not  contiguous  to  the  ventral  lobes. 
Two  kinds  of  pneumonia  are  encountered,  namely,  lobar 
and  catarrhal  or  broncho-pneumonia.  In  the  former  the  vesi- 
cular portion  of  the  lung  substance  is  chiefly  affected  ;  in  the 
latter  the  smaller  bronchioles  are  primarily  attacked  and  the 
alveoli  secondarily.  In  croupous- pneumonia,  there  is,  follow- 
ing the  stage  of  congestion,  an  emigration  of  red  blood  cor- 
puscles, some  leucocytes,  and  an  exudate  of  fibrin  into  the  air 
spaces.  These  elements  are  firmly  matted  together  by  the 
coagulating  fibrin,  making  the  diseased  lung  firm  to  the  touch. 
In  broncho-pneumonia  the  catarrhal  condition  of  the  smaller 
air  tubes  makes  them  impervious  to  air.  The  lung  tissue 
which  they  supply  is  gradually  emptied  of  air  and  assumes  the 
appearance  of  red  flesh,  owing  to  the  collapse  of   the  walls  of 


Fig.  10. 


Portion  of  a  pig's  lung  showii 
emphysema. 


ISrORBID      ANATOMV 


79 


the  alveoli  and  the  distended  condition  of  the  capillary  net- 
work. Subsequently  the  inflammation  extends  into  the  alveoli, 
which  then  become  distended  with  cellular  masses. 

The  nature  of  the  lung  disease  will  depend  more  or  less 
upon  the  mode  of  entrance  of  the  virus.  If  it  enters  only 
by  way  of  the  air  tubes  it  will  appear  perhaps  as  a  broncho- 
pneumonia. If  it  enters  the  lung  tissue  through  the  circula- 
tion we  may  have  more  or  less  scattered  centers  of  hepatiza- 


FiG.  II.  Right  lung  of  pig.  The  stippled  portion  is  usually 
involved  in  cases  of  infectious  pneumonia  or  sivine  plague.  {/>)  ventral 
lobe,  {c)  cephalic  lobe,  {a) principal  lobe.  The  ventral  lobe  is  usually 
the  seat  of  the  more  advanced  disease  and  consequently  the  first  to  become 
hepafized.  The  cephalic  portion  of  the  principal  lobe  (.r)  is  usually 
hepatized  and  the  reinaining  portion  deeply  reddoied. 

tion  (embolic  pneumonia).  If  it  enters  by  way  of  the  pleura, 
the  virus  will  creep  along  the  interlobular  and  peribronchial 
tissue  before  it  invades  the  parenchyma  proper. 

In  natural  infection  of  swine  plague,  bacteria  seem  to 
enter  the  lung  tissue  chiefly  by  way  of  the  air  tubes.  At  the 
same  time  it  is  not  improbable  that  occasionally  they  may 
enter  the  serous  cavities  first,  /.  e. ,  invade  the  pleural  cavities 
and  thence  the  lungs.     This  probability  is  shown  by  inocula- 


8o  SWINE     PLAGUE 

tion  in  which  intravenous  injections  produced  exudative  pleu- 
ritis  and  pneumonia  of  the  most  dependent  portions  of  the 
lungs  covered  by  the  pleural  exudate.  It  is  not  improbable 
that  even  in  the  natural  disease  the  bacteria  which  have 
gained  access  to  a  portion  of  the  lung  tissue  by  way  of  the  air 
tubes  reach  the  pleura  covering  this  portion,  and  may  then  by 
this  route  invade  other  portions  of  the  lungs.  It  may  be  that 
in  this  way  a  pneumonia  originally  single  may  become  double. 
It  has  been  observed  that  the  first  pneumonic  infiltration  of 
the  principal  lobe  was  at  the  point  of  contact  with  the  dis- 
eased ventral  lobe,  and  that  the  resting  of  a  lobe  against  an 
inflamed  serous  surface,  such  as  the  pericardium,  caused  a 
pneumonic  infiltration  at  the  point  of  contact. 

The  character  and  seat  of  the  lung  lesions  are  somewhat 
variable.  It  is  difficult  to  find  two  lungs  exactly  alike  so  far 
as  gross  appearances  go.  This  to  be  sure  may  be  due  largely 
to  the  fact  that  animals  die  in  different  stages  of  the  disease. 
Yet  there  are  differences  evidently  not  dependent  on  this  fact, 
which  must  be  left  for  special  pathological  investigation. 

In  general  the  cephalic  (anterior)  half  of  a  swine-plague 
lung  is  hepatized,  of  a  dark-red  or  grayish-red  color  and  firm 
to  the  touch.  The  pleura  is  more  or  less  thickened  and 
opaque,  and  possibly  covered  with  easily  removable,  friable, 
false  membranes.  In  the  more  recently  affected  regions  a 
faint  but  quite  regular,  delicate  mottling  with  yellow  is 
observed  to  shine  through  the  pleura  when  not  thickened. 
These  minute  hazy,  yellowish  dots  usually  occur  in  groups  of 
four.  Occasionally  whitish  or  yellowish  patches  varying 
much  in  size  are  seen,  perhaps  more  frequently  in  the  ventral 
lobes.  These  correspond  to  homogeneous  dead  masses  of  lung 
tissue. 

When  such  lungs  are  cut  open,  the  section  presents  much 
the  same  appearance,  both  as  regards  color  and  mottling,  as 
when  viewed  from  the  surface,  excepting  that  the  details  are 
less  distinct.  In  some  cases,  in  the  most  recently  invaded 
territories  in  the  principal  lobe  and  nearer  the  dorsum  in  the 
other  lobes,  the  dark  or  grayish-red  cut  surface  shows  grayish 


MORBID    ANATOMY  3j 

lines  usual]}'  arranged  in  curves  and  circles.  These,  so  far  as 
determined,  represent  the  cut  outlines  of  the  interlobular  and 
peribronchial  tissue  infiltrated  with  cells.  It  has  already  been 
stated  that  these  lines  may  represent  the  paths  along  which 
the  swine- plague  bacteria  invade  the  lungs  from  the  pleural 
surface. 

The  cut  ends  of  the  bronchi  of  the  ventral  lobes  are  fre- 
quently occluded  with  thick,  whitish  pus  ;  in  the  other  lobes 
a  reddish  froth  is  usually  present.  Rarely  they  also  contain 
thick  glairy  mucus  in  which  particles  of  dry  pus  and  lung 
worms  are  imbedded.  The  contents  of  the  air  tubes  in  the 
ventral  lobes  may  have  been  derived  from  the  overdistended 
alveoli,  or  else  a  broncho-pneumonia  may  have  preceded  the 
swine-plague  pneumonia. 

In  microscopic  sections  of  diseased  lung  tissue  the  alveoli 
and  smallest  air  tubes  are  found  distended  with  cell  masses 
consisting  chiefly  of  leucocytes.  Usually  there  is  very  little 
fibrin  and  very  few  red  corpuscles  in  the  alveoli,  even  in  cases 
in  which  the  disease  was  quite  recent.  It  may  be  that  the 
stage  represented  in  ordinary  croupous-pneumonia  by  the  pres- 
ence of  fibrin  in  connection  with  the  cellular  elements  is  very 
brief,  and  that  it  is  speedily  replaced  by  large  numbers  of  leu- 
cocytes. The  large  predorainence  of  these  elements  in  some 
portions  of  the  lungs,  as  well  as  beginning  fatty  degeneration, 
is  probably  the  cause  of  the  regular  mottling  of  the  lungs,  as 
seen  from  the  surface.  The  little  yellowish  hazy  dots  represent 
alveoli  surrounded  by  the  hyperemic  walls. 

The  necrotic  and  caseous  changes  so  frequent  in  swine 
plague  are  most  interesting.  The  latter  are  usually  quite  small 
and  disseminated  in  large  numbers  over  the  diseased  lobes. 
The  former  represent  larger  masses  from  a  marble  to  a  horse- 
chestnut  in  size.  They  represent  tissue  which  has  been 
destroyed  by  the  rapid  multiplication  of  .swine-plague  bacteria 
in  particular  localities.  Hence  they  are  found  in  all  stages  of 
the  pneumonia.  The  large  caseous  masses  may  be  considered 
as  the  result  of  a  slow  death  of  larger  areas  of  lung  tissue,  due 
primarily  to  the  gradual  overdistention  of  the  tissue  bv   leuco- 


82 


SWINE    PLAGUE 


cytes,  and  hence  the  gradual  cutting  off  of  the  blood  supply. 
One  is  a  rapid  death  due  directly  to  highly  virulent  bacteria, 
the  other  a  slow  death,  or  a  kind  of  dry  suppuration  in  the 
later  stages  of  the  pneumonia,   characteristic  of  the  pig,    and 

due  indirectly  to  the 
irritation  of  perhaps 
more  attenuated  races 
of  bacteria.  In  some 
cases  there  are  exten- 
sive hemorrhages  in 
the  interlobular  con- 
nective tissue. 

The  inflammation 
of  the  pleura  fre- 
quently extends  to  the 
pericardium.  This 
membrane  is  opaque, 
thickened  and  its  ves- 
s  e  1  s  distended.  It 
may  be  glued  to  the 
contiguous  lobes  of 
the  lungs  and  covered 
by  a  false  membrane,  smooth  or  roughened,  which  extends 
upon  the  large  vessels  emerging  at  its  base. 

Disease  of  the  digestive  tract  in  a  considerable  proportion 
of  animals  inoculated  with  swine-plague  cultures  consisted 
n  a  severe  catarrhal  inflammation  of  the  lining  membrane 
of  the  stomach.  The  hyperemia  was  very  intense,  bordering 
on  hemorrhage.  Occasionally  the  extension  of  the  peritonitis, 
produced  by  intra-abdominal  inoculation  along  the  mesenterj'^, 
causes  a  severe  inflammation,  with  exudation  on  the  mucosa 
of  the  small  intestine.  A  case  is  reported  where  all  the  Peyer's 
patches  of  the  small  intestine  were  in  a  hyperemic  and  partly 
hemorrhagic  condition. 

In  the  naturally  contracted  disease  extensive  hyperemia 
of  the  mucosa  of  the  large  intestine,  bordering  on  a  hemor- 
rhagic condition,  has  been  observed.     In  other  cases  a  peculiar 


Fig.  12.  Hemorrhage  in  the  interlobular 
tissue  of  a  sivine-plague  king:  (a)  hemor- 
rhage, {b)  hepatized  lobules. 


MORBID    ANATOMY  83 

croupous  exudation  appeared,  which  seemingly  resulted  from 
the  effect  of  swiue-plague  bacteria  in  the  large  intestine. 

The  production  of  intestinal  disease  by  swine-plague  bac- 
teria may  be  supposed  to  go  on  as  follows  :  the  bacteria  first 
attack  the  lung  tissues  and  there  produce  more  or  less  hepatiza- 
tion. The  blood  through  the  lungs  finds  its  path  partly  ob- 
structed. This  reacts  on  the  blood  in  the  right  side  of  the 
heart  and  the  venous  blood  entering  it.  Hence  there  may  be 
more  or  less  stasis  of  blood  in  the  portal  circulation  which  in 
turn  impairs  the    digestive   functions    of  the    stomach.     The 


Fig.  13.     Kidney  from  a  case  of  acute  szvine  plague,  shozcing  punc- 
ti for  111  hemorrhages. 

swine-plague  bacteria  in  the  lungs  in  the  later  stages  of  the 
pneumonia  may  be  coughed  up  in  the  contents  of  the  bronchial 
tubes,  swallowed  and  passed  through  the  impaired  stomach 
unharmed  into  the  intestines.  The  stagnation  of  the  feces  in 
the  large  intestine  furnishes  the  bacteria  an  opportunity  to 
cause  inflammation  with  exudation  on  the  mucous  membrane. 
The  tendency  of  swine-plague  bacteria  to  cause  fibrinous 
inflammatory  deposits  on  serous  membranes  may  serve  to 
explain  such  action  on  mucous  membranes. 

There  is  general  congestion  with  resulting  degeneration 
of  the  parenchyma  of  the  spleen,  kidneys  and  liver  in  the  acute 
septicemic  forms  of  the  disease.     In  these  cases  the  specific 


84  SWINE     PLAGUE 

bacterium  is  easily  obtained  from  the  abdominal  organs.  In 
brief,  the  lesions  of  swine  plague  as  they  appear  in  various 
outbreaks  may  be  summarized  in  four  classes,  namely  : 

1.  The  acute  septicemic  form  in  which  the  lesions  are 
characterized  by  a  general  hyperemic  condition  of  the  serous 
membranes  and  parenchymatous  organs.  Not  infrequently 
hemorrhages,  especially  the  punctiform  variety,  occur.  No 
localized  lesions. 

2.  Cases  of  pneumonia  with  or  without  pleuritis.  The 
other  organs  remained  normal  in  appearance. 

3.  Cases  where  either  in  addition  to,  or  possibly  in  the 
absence  of,  the  lung  lesions  there  are  marked  anatomical 
changes  in  the  mucosa  of  the  digestive  tract  and  possibly  in 
the  lymphatic  glands. 

4.  Cases  of  mixed  infection,  especially  with  hog  cholera, 
where  in  addition  to  the  swine-plague  lesions  which  may  be 
more  or  less  modified,  there  are  those,  especially  of  the  diges- 
tive tract,  characteristic  of  the  accompanying  disease. 

In  order  to  present  as  clear  a  picture  as  possible  of  the 
findings  in  a  case  of  this  disease,  the  published  autopsy  notes 
of  one  animal  are  appended. 

"Pig  died  yesterday,  put  on  ice.  Weight  about  30  pounds.  Skin 
on  ventral  aspect  of  body  more  or  less  reddened  ;  over  the  sternum  a 
few  excoriations.  The  enlarged  inguinal  glands  show  as  lumps  under 
the  skin.  On  section  they  present  a  mottled  gray  and  red  surface,  the 
red  limited  chiefly  to  the  cortex.  Edema  of  the  subcutis  over  right 
knee. 

"  False  membrane  covers  the  left  half  of  the  mass  of  intestines  and 
the  spleen  ;  consists  of  an  elastic,  rather  firm  yellowish  white  layer. 
Spleen  firmly  glued  to  the  surrounding  intestines,  slightly  enlarged, 
dark,  softened.  Liver  firm,  cut  with  considerable  difficulty.  Kidneys 
in  condition  of  parenchymatous  degeneration.  One  hemorrhagic  spot 
in  medullary  portion  of  the  kidney.  Pelvis  contains  a  whitish  glairy 
liquid. 

"  Digestive  tract.  Two  superficial  necroses  on  the  inner  surface  of 
lower  lip  in  front,  one  on  the  upper  lip  and  on  edge  of  tongue  near  tip. 
Stomach  contains  a  little  deeply  bile-stained  fluid.  Mucosa  sprinkled 
with  red  spots  of  a  washed-out  appearance,  most  numerous  in  fundus 
and  near  pyloric  valve.     Hyperemia  of   duodenum   begins   sharply  at 


MORBID    ANATOMY  85 

pyloric  valve.  From  the  opening  of  bile  duct  a  few  drops  of  thick  bile 
can  be  expressed.  Remainder  of  small  intestine  not  markedly 
changed.  The  Peyer's  patch  in  lower  ileum  has  some  of  its  follicles 
enlarged  from  which  caseous  masses  can  be  expressed. 

"Large  intestine  contains  much  sand  and  gravel.  Mucosa  of 
caecum  of  a  dark  slate  color.  The  summit  of  the  folds  of  a  puri)lish 
hue.  Free  edge  of  valve  bordered  by  a  thin  slough.  On  Feyer's  patch 
near  valve  areas  of  necrotic  tissue  of  a  yellowish  color,  resting  on  a 
firm,  yellowish-white  base  three-sixteenths  of  an  inch  thick.  Upper 
colon  has  its  mucosa  of  the  same  dark  slate  color,  merging  into  a  wine 
red.  Two  ulcers  one-eighth  of  an  inch  in  diameter  observed.  In  lower 
colon  congestion  slight  and  gradually  disappearing  towards  rectum.  A 
small  number  of  circular  whitish  erosions,  apparently  associated  with 
the  solitary  follicles. 

"Thorax.  On  the  left  lung,  the  ventral  and  cephalic  lobes  are  in- 
terspersed with  small  regions  of  collapse.  The  remainder  of  the  lobes 
very  emphysematous  and  hyperemic.  Of  the  right  lung,  the  anterior 
half  (/.  e.,  including  cephalic,  ventral,  and  adjacent  portion  of  principal 
lobes)  hepatized,  covered  by  a  thin  false  membrane,  gluing  the  various 
lobes  lightly  to  each  other  and  to  chest  wall.  The  diseased  lobes  show 
the  regular  mottling  in  the  upper,  dorsal  portion.  As  we  proceed  to- 
wards the  ventral  portion  the  mottling  is  less  distinct,  the  tissue  firmer 
and  interspersed  with  small,  irregular,  necrotic  foci.  The  smaller 
bronchi  contain  a  thick,  whitish  pus.  In  ventral  lobe  a  portion  of  the 
parenchyma  as  large  as  a  marble  completely  converted  into  a  grayish- 
yellow  homogeneous  mass.  Of  the  principal  lobe  about  one-third  or 
one-fourth  hepatized.  The  mottling  of  surface  very  regular.  On  sec- 
tion grayish,  circumscribed  areas  one-half  an  inch  in  diameter  inter- 
spersed. Over  tnese  masses  the  pleura  is  converted  into  a  wrinkled, 
roughened,  hide-like  membrane. 

"  Trachea  and  bronchi  contain  small  quantities  of  foamy  liquid  in- 
termingled with  yellowish  particles.  Bronchial  glands  barely  enlarged, 
firm  ;  some  lobules  pale,  others  reddened. 

"Bacteriological  notes.  At  the  autopsy  an  agar  tube  was  inoculated 
with  a  platinum  loop  lightly  rubbed  over  the  pleural  exudate.  On  the 
following  day  a  thin  grayish  growth  with  condensation  water  clouded. 
Examination  of  hanging  drop  and  stained  cover-glass  preparations  shows 
only  swine-plague  germs. 

"In  cover-glass  preparations  of  hepatized  lung  tissue  a  large  number 
of  germs  resembling  swine-plague  bacteria  were  seen. 

"With  a  bit  of  hepatized  lung  tissue,  a  rabbit  was  inoculated  subcu- 
taneouslyat  2  p.  m.  The  rabbit  was  dead  next  morning  at  8  .\.  m.,  /.  e., 
in  less  than  18  hours.     In  spleen,  liver,  and   blood  preparations  nunier- 


86  SWINE     PLAGUE 

ous  pular-stained  swine-plague  germs  present.       An  agar   culture   from 
heart's  blood  contained  only  swine-plague  germs. 

"From  the  peritoneal  exudate  of  pig,  consisting  of  cells  and  fibrin 
and  numerous  bacteria  of  several  varieties,  two  agar  plate  cultures  were 
made.  On  Plate  A  one  large  colony  of  spore-bearing  bacilli  and  one 
small  colony  of  swine-plague  germs.  Plate  B,  completely  overgrown 
by  the  spore -bearing  bacillus. 

"A  bouillon  culture  from  the  exudate  contains  streptococci  and 
swine-plague  bacteria.  Agar  plate  cultures  were  made  therefrom  and 
both  germs  isolated. 

"At  the  same  time  a  large  rabbit  was  inoculated  subcutaneously 
with  a  bit  of  the  exudate.  Dead  in  18  hours.  Stained  cover-glass  pre- 
parations of  blood  from  heart,  spleen  and  liver  tissue  show  polar- 
stained  swine-plague  germs.  An  agar  culture  from  the  blood  contains 
only  swine-plague  germs. 

"From  the  spleen,  after  thoroughly  scorching  through  the  exudate, 
two  agar  plate  cultures  and  a  bouillon  culture  were  made  with  bits  of 
spleen  pulp.  The  bouillon  culture  contained  only  swine-plague  germs. 
"The  swine-plague  bacteria  were  thus  obtained  from  lungs,  pleura, 
spleen,  and  peritoneal  exudate,  while  hog-cholera  bacilli,  which  were 
looked  for  with  the  greatest  care,  could  not  be  found."  (Smith, 
Report  on  Swine  Plague,  p.  62. ) 

The  course  of  the  disease  varies  in  acute  cases  from  one  to 

three  weeks.     In  chronic  or  complicated  cases  it   is  indefinite. 

The  prognosis  in  swine  plague  is  very  unfavorable.      Most 

of  the  affected  animals  die.  and  tho.se  that  recover  are   usually 

not  thrifty. 

§  72.  Differential  diagnosis.  In  sporadic  cases,  swine 
plague  is  to  be  differentiated  from  broncho-pneumonia  due  to 
other  causes  than  the  swine-plague  bacterium.  Pneumonia  of 
a  non  specific  nature  is  often  associated  with  deaths  due  to 
dietary  or  other  causes.  It  frequently  causes  death  in  chronic 
cases  of  other  diseases  (terminal  pneumonia). 

In  epizootics  or  outbreaks,  it  is  to  be  distinguished  from 
hog  cholera  when  there  is  accompanying  catarrhal  pneumonia. 
To  make  a  positive  diagnosis,  it  is  usually  necessary  to  depend 
upon  the  results  of  the  bacteriological  examination. 

Pneumonia  resulting  from  lung  worms  {Strongylus  para- 
doxus) can  be  distinguished  by  a  careful  examination  of  the 
contents  of  the  bronchioles. 


PREVENTION  87 

In  case  of  coexistence  of  hog  cholera  and  swine  plague  a 
bacteriological  examination  is  necessary  to  determine  the  pres- 
ence of  the  two  diseases,  owing  to  the  possibility  of  an  accom- 
panying or  terminal  pneumonia  with  hog  cholera. 

The  question  has  arisen  as  to  whether  the  presence  of  Bad. 
septicemiae  hcmorrhagicae  in  the  hepatized  lung  constitutes  a 
diagnosis  of  swine  plague.  As  understood  at  the  present  time 
it  would  seem  that  the  presence  of  this  species  of  bacteria 
would  indicate  the  nature  of  the  disease.  It  must  be  remem- 
bered, however,  that  bacteria  not  readily  distinguishable  from 
swine-plague  organism  exists  in  the  normal  upper  air  passages, 
from  whence  it  could  be  brought  into  the  lung  and  in  such  a 
case  it  might  appear  as  a  secondary  invader  only,  or  it  might 
have  been  primarily  the  cause  of  the  lesions.  It  is  not  improb- 
able that  epizootics  may  start  from  these  sporadic  cases, 
although  conclusive  proof  of  this  is  still  wanting.  It  seems, 
however,  that  the  presence  of  this  organism  in  the  lung  tissue 
of  a  sporadic  case  should  be  considered  in  the  light  of  the  dis- 
tribution of  these  organisms  and  not  necessarily  as  the  starting 
of  an  epizootic. 

§73,  Prevention.  Recent  investigations  show  that  out- 
breaks of  swine  plague  are  much  more  extensive  than  hereto- 
fore supposed.  The  present  knowledge  of  this  disease  indi- 
cates that  the  adoption  of  measures  for  its  prevention  is  quite 
as  important  as  for  hog  cholera.  In  general  the  measures  to 
be  adopted  and  followed  and  the  rules  to  be  observed  in  the 
prevention  of  epizootic  swine  plague  are  practically  the  same 
as  those  for  the  prevention  of  hog  cholera.  It  will  be  seen 
from  a  comparison  of  the  two  species  of  bacteria  that  the 
bacillus  of  hog  cholera  is  a  more  hardy  organism  than  that  of 
swine  plague.  Thus  the  swine-plague  bacterium  is  destroyed 
more  rapidly  by  drying  and  will  live  a  much  shorter  time  in 
the  soil.  However,  the  channels  through  which  it  may  gain 
access  to  a  herd  are  practically  the  same,  and  every  precaution 
suggested  in  reference  to  hog  cholera,  is  applicable  to  swine 
plague.     It  is  believed  that  the  time  during  which  a  field,  hog 


88  SWINE     PLAGUE 

3-ard  or  pen  should  be  kept  free  from  swine  after  the  appear- 
ance of  the  disease  can,  with  safety,  be  shorter  after  swine 
plague  than  after  hog  cholera.  In  any  case  several  months 
should  elapse  before  the  yards  or  pens  are  reoccupied.  If  the 
disease  appears,  the  well  animals  should  be  promptly  separated 
from  the  sick  and  placed  in  suitable  pens  or  yards,  protected 
against  subsequent  infection,  and  given  an  abundance  of 
wholesome  food  and  water.  It  is  well  to  remove  the  sick 
animals  to  other  pens.  The  thorough  disinfection  of  the 
infected  pens  should  be  insisted  upon  before  they  are  again 
occupied. 

v^  74.  Specific  treatment.  For  a  number  of  years 
investigations  were  almost  constantly  under  way  in  the  United 
States  Bureau  of  Animal  Industry,  for  the  purpose  of  finding 
some  method  by  which  the  disease  could  be  successfully  and 
specifically  treated.  Drugs  and  medicines  have  been  tried, 
preventive  inoculations  and  injections  of  toxins  have  been 
made.  The  serum  therapy  which  has  effected  relief  in  certain 
other  diseases  has  been  and  is  now  being  tested  with  some- 
what favorable  results,  by  a  few  European  workers,  yet  we  do 
not  see  that  a  specific  therapeutic  agent  has  been  demon- 
strated. In  view  of  this,  it  becomes  necessary  to  apply  with 
renewed  zeal  our  present  knowledge  of  the  nature  of  the 
malady  and  endeavor  to  prevent  its  occurrence  or  reappear- 
ance by  keeping  the  animals  under  the  best  possible  condi- 
tions. Prevention  of  this  disease  is  more  promising  than  its 
treatment. 

§  75.  The  effect  of  swine-plague  bacteria  in  rabbits. 
In  1894,  Smith  and  Moore  described  the  appearance  of  the 
effect  of  swine-plague  bacteria  in  rabbits  and  also  the  effect  of 
resistance  on  the  part  of  the  rabbit  on  the  form  of  the  resulting 
lesions.  As  this  disease  is  caused  by  a  bacterium  belonging 
to  the  septicemia  hemorrhagica  group,  it  seems  desirable  that 
the  results  above  referred  to  should  be  restated.  The  appended 
paragraphs  are  taken  from  the  report  of  these  investigations. 

Among  the   forms  of  disease  observed  after  the   subcu- 


EFFECT    ON    RABBITS  89 

taneous  inoculation  of  rabbits  with  swine-plagne  bacteria  from 
different  sources  (epizootics)  are  the  following  : 

1.  Septicemia. 

2.  Peritonitis. 

3.  Pleuritis  (usually  with  pericarditis). 

4.  Pleuritis  (usually  with  pericarditis  and  peritonitis). 

5.  Local  lesion  onh'. 

In  septicemia,  death  ensues  within  eighteen  or  twenty- 
four  hours.  The  local  lesion  produced  at  the  seat  of  inocula- 
tion is  slight.  Bacteria  are  abundant  in  the  parenchyma 
(blood  ve.ssels)  of  the  various  organs.  In  the  form  character- 
ized by  peritonitis  death  ensues  in  three  to  seven  days.  The 
local  lesion,  which  in  all  these  forms  of  diseases  increases  in 
extent  with  the  prolongation  of  the  life  of  the  animal,  is  here 
characterized  by  more  or  less  suppurative  infiltration  of  the 
skin  and  the  subcutis.  The  peritonitis  in  its  earlier  stages  is 
characterized  by  punctiform  hemorrhages  on  the  cecum  'and 
a  fibrinous  or  cellular  exudate.  It  always  contains  immense 
numbers  of  bacteria.  When  pleuritis  is  also  present  the  exu- 
date usually  involves  the  pericardium  as  well.  It  varies  in 
amount  according  to  the  duration  of  the  disease  and  is  essen- 
tially the  same  as  the  peritoneal  exudate. 

The  form  characterized  by  pleuritis  and  pericarditis  with- 
out peritonitis  is  interesting  in  so  far  as  the  seat  of  inoculation 
does  not  explain  the  localization,  for,  in  every  case,  the  inocu- 
lation was  made  in  the  region  of  the  abdomen.  The  lungs 
may  become  hepatized  secondarily  through  invasion  from  the 
pleura  if  the  animal  lives  long  enough. 

Lastly,  the  form  of  disease  in  which  the  only  localization 
is  a  very  extensive  suppurative  infiltration  associated  with 
hemorrhage  and  edema  of  the  subcutaneous  tissue  is  not 
common. 

It  should  be  stated  that  the  cultures  from  the  same  out- 
break continued  to  produce  the  same  form  of  disease  in  rab- 
bits until  modified  by  age.     The  maintenance  of  a  certain  uni- 


go  SWINE   PLAGUE 

form  virulence  for  years  is  well  exemplified  by  a  variety  iso- 
lated in  the  summer  of  1890.  This  variety  was  fatal  to 
rabbits  within  twenty  hours  when  first  isolated  and  this 
degree  of  virulence  maintained  itself  for  a  period  of  nearly 
four  years. 

§  76.  Modifications  of  the  septicemic  type  by  in- 
creasing the  resistance  of  rabbits.  By  the  injection  of  steril- 
ized cultures  which  increase  the  resistance  of  rabbits,  Smith 
and  Moore  were  able  to  produce  nearly  all  the  pathological 
variations  which  follow  the  inoculation  of  natural  races  of 
swine-plague  bacteria  as  isolated  from  outbreaks.  This  modi- 
fication of  the  septicemic  type  is  not  fortuitous,  for  among  the 
large  number  of  rabbits  inoculated  during  three  and  one- 
half  years  with  the  culture  employed,  none  survived 
twenty  to  twenty-four  hours.  Whenever  the  course  of  the 
inoculation  disease  in  rabbits  departed  from  this  rapidly  fatal 
type,  it  was  due  to  some  preliminary  treatment  of  the  rabbit. 

The  degree  of  resistance  determined  quite  regularly 
though  not  invariably  the  form  of  the  disease.  This  degree 
was  measured  by  the  relative  quantity  of  the  protective  ma- 
terial (sterilized  cultures,  sterilized  blood,  and  blood  serum) 
injected.  The  grades  of  disease  induced  range  themselves  in. 
the  following  order  : 

No  resistance — acute  septicemia. 
Slight  resistance — peritonitis. 

Increased  resistance — pleuritis  and  pericarditis  with  or  with 
out  secondary  pneumonia. 

4.  Higher  degree  of  resistance—  pleuritis  and  peritonitis. 

5.  Still  greater  resistance — irregular  lesions  in  the  form  of  ab- 
scesses, subcutaneous  and  subperitoneal. 

Nearly  complete  immunity.     Very   slight   reaction   at   the 
point  of  inoculation. 

Most  of  the  cases  cited  below  as  illustrating  these  modified 
forms  of  the  septicemic  type  belong  to  the  series  of  immuniz- 
ing experiments  of  the  preceding  article.  To  this  the  reader 
is  referred  for  additional  illustrations. 


MODIFICATIONS 


91 


First  degree  0/  resistatia— peritonitis. — Rabbit  No.  12  re- 
ceived 7  cc.  of  bouillon  culture  of  swine-plague  bacteria  steril- 
ized b)'  heat.  Subsequently  with  a  control  rabbit  it  was  in- 
oculated with  a  minute  dose  of  swine-plague  bacteria  under 
the  skin.  The  control  died  within  eighteen  hours,  the  treated 
rabbit  in  three  days.  The  macroscopic  changes  were  limited 
to  the  point  of  inoculation  and  the  peritoneum.  At  the  former 
there  was  a  purulent  infiltration  of  the  subcutis,  1.5  cm.  in 
diameter,  with  a  dilation  of  surrounding  blood  vessels.  The 
peritonitis  was  characterized  by  an  exudate  of  a  slightly  viscid 
character  covering  liver,  spleen,  and  cecum,  and  made  up  of 
fibrin,  leucocytes  and  immense  numbers  of  bacteria. 

Second  degree  of  resistance— pleiiritis  and  pericarditis. — Rab- 
bit No.  38  was  treated  before  inoculation  with  4.5  cc.  of  a 
sterilized  suspension  of  agar  cultures  of  swine-plague  bacteria 
in  3  doses.  Together  with  a  control  rabbit,  it  received  under 
the  skin  the  equivalent  of  o.ooi  cc.  of  a  fresh  bouillon  culture 
of  swine-plague  bacteria.  The  control  died  in  twenty  hours. 
The  treated  rabbit  died  six  days  after  inoculation.  At  the 
point  of  inoculation  there  was  a  purulent  infiltration  of  the  sub- 
cutis 3  cm.  in  diameter.  The  abdomen  and  abdominal  viscera 
were  free  from  macroscopic  changes.  In  the  thorax,  the  pleural 
cavity  was  lined  with  a  grayish,  friable  exudate  consisting  of 
round  cells  and  bacteria.  Lungs  hyperemic  and  only  partly 
collapsed.     Pericardium  also  covered  with  a  slight  exudate. 

Tliird  degree  of  resistance — pleuritis  (^pericarditis)  a7id peri- 
tonitis.— Rabbit  No.  15  received  in  the  ear  vein  a  total  of  12  cc. 
of  a  sterilized  bouillon  culture  of  swine-plague  bacteria.  It  was 
inoculated  subcutaneously  with  virulent  swine-plague  bacteria 
May  26,  and  died  June  3,  eight  days  later.  The  control  rabbit 
died  within  eighteen  hours.  The  following  changes  were 
observed  : 

A  purulent  infiltration  into  the  subcutaneous  tissue  at  the  point  of 
inoculation  extending  over  an  area  6  cm.  in  diameter.  The  superficial 
layer  of  the  subjacent  muscle  discolored.  Surrounding  the  area  of 
infiltration  the  blood  vessels  were  injected.  The  cecum  and  liver 
were    covered    with    a    very    thin    grayish    exudate,    which    also  ap- 


92  SWINE    PLAGUE 

peared  on  and  between  the  coils  of  the  intestine.     vSpleen  not  enlarged. 

The  right  lung  and  chest  wall  covered  with  a  thin  grayish  exudate. 
In  the  cephalic  lobe,  two  small  areas  of  consolidation  ;  principal  lobe 
hyperemic.  The  left  pleural  cavity  lined  with  a  quite  thick  membran- 
ous exudate,  which  covered  the  entire  surface  of  the  lung.  On  the  dor- 
sal surface  of  the  principal  lobe  a  mass  of  lung  tissue  2  cm.  in  diameter, 
firm  and  of  a  yellowish-gray  color.  The  remaining  portion  of  the  prin- 
cipal lobe  hyperemic  ;  cephalic  lobe  in  a  state  of  collapse. 

Pericardium  covered  with  a  thin  cellular  exudate. 

Higher  degrees  of  resistance. — None  of  the  treated  animals 
which  have  come  under  our  observation  have  succumbed  to  a 
mere  extension  of  the  lesion  produced  at  the  point  of  inocula- 
tion as  is  occasionally  observed  after  inoculation  with  certain 
varities  of  swine-plague  bacteria  found  in  nature.  There  have 
been  noticed,  however,  certain  peculiar  localizations  resem- 
bling those  produced  in  the  subcutis  after  inoculation,  and  in 
a  few  cases  the  local  lesion  persisted  a  considerable  length  of 
time.  It  was  quite  severe  in  all  fatal  cases  in  which  the  disease 
was  prolonged  several  weeks  after  inoculation,  although  the 
real  cause  of  death  was  due  in  all  such  cases  to  localizations  on 
one  or  more  of  the  serous  membranes.  The  peculiar  forms  of 
disease  may  be  grouped  as  follows  : 

(a)  Persistence  of  local  lesiofis. — Rabbit  No.  50  received  in  the 
abdominal  cavity  3.5  cc.  of  the  sterilized  suspension  of  agar  cultures  in  3 
doses.  It  was  subsequently  inoculated  beneath  the  skin  with  o.ooi  cc. 
of  a  bouillon  culture  of  swine-plague  bacteria  which  produced  a  large 
local  swelling.  On  February  25,  1892,  nearly  eight  months  after  its 
inoculation,  it  was  chloroformed.  The  only  lesion  found  was  in  the 
subcutaneous  tissue.  At  the  point  of  inoculation  the  skin  was  sloughed 
over  an  area  3  cm.  in  diameter.  The  denuded  surface  was  covered  with 
a  thick  scab.  The  subcutis  beneath  the  scab  and  surrounding  the  ulcer 
was  infiltrated  with  pus.  A  stained  cover-glass  preparation  showed 
swine-plague  bacteria.     No  other  lesions  were  found. 

{b)  Sub-peritoneal  abscess.— ^ahhit  No.  16  was  injected  intraven- 
ously with  16  cc.  of  sterilized  bouillon  cultures  of  swine-plague  bacteria. 
After  some  days  it  was  inoculated  beneath  the  skin  with  o  001  cc.  of  a 
fresh  bouillon  culture  of  virulent  swine-plague  bacteria.  The  control 
rabbit  died  within  twenty  hours.  Rabbit  No.  16  showed  no  ill  effect 
from  the  inoculation  for  several  months,  when  it  was  noticed  that  it  was 
becoming  emaciated.  It  died  June  11,  1892,  one  year  and  six  davs  after 
its  inoculation,  with  a  subperitoneal  abscess. 


RESISTANCE  IN  RAB15ITS 


93 


(c)  Mjiltiple  abscesses  under  the  skin.  —Rabbit  No. 439  received  into 
the  ear  vein  in  three  injections  4  cc.  of  sterilized  blood  from  a  swine 
plague  rabbit.  Later  it  was  inoculated  subcutaneously  with  o.ooi  cc.  of 
a  bouillon  culture  of  virulent  swine-plague  bacteria.  The  control  rabbit 
died  within  twenty  hours.  Two  months  after  the  inoculation  it  was 
noticed  that  this  rabbit  with  others  was  suffering  from  a  large  number 
of  subcutaneous  abscesses. 

REFERENCES. 

1.  DE  vSCHWEiNiTz.  vSerum  therapy.  Proceedings  Society /or  the 
Promotion  0/  Agricultural  Science,  1896,  p.  47. 

2.  DE  ScHWEiNiTz.  The  serum  treatment  of  swine  plague  and 
hog  cholera.     Bulletin  No.  23,  U.  S.  Bureau  0/  Aniinal  Industry,  1899. 

.V  Evans.  Hamorrhagische  septikjimie  des  elephanten.  The 
Jour,  of  Tropical  Vet.  Science,  Vol.  i,  p.  283. 

4.  JOEST.     Schweineseuche  und  Schweinepest.    Jena,  1906. 

5.  IvOEFFLER.  Arbeiten  a.  d.  Kaiserlichen  Gesundheitsainte,  Bd. 
I  (1885),  S.  51. 

6.  Moore,  Pathogenic  and  toxicogenic  bacteria  in  the  upper  air 
passages  of  domesticated  animals.  Bulletin  No.  j.  U.  S.  Bureau  of 
Animal  Industry,  1893. 

7.  Moore.  Concerning  the  nature  of  infectious  swine  diseases  in 
the  State  of  New  York  with  practical  suggestions  for  their  prevention 
and  treatment.  Report  of  the  Neiv  York  State  Commissioner  of 
Agriculture,  1897. 

8.  Smith.  Preliminary  investigations  concerning  infectious  pneu- 
monia in  swine  (Swine  plague).  Ann.  Rpt.  Bureau  of  Animal  In- 
dustry, U.  S.  Dept.  of  Agriculture,  1886,  p.  76. 

9.  Smith.  Special  report  on  swine  plague.  Bureau  of  Animal 
Industry,  (J.  S.  Dept.  of  Agriculture,  1891. 

10.  Smith  and  Moore.  Experiments  on  the  production  of  im- 
munity in  rabbits  and  guinea  pigs  with  reference  to  hog-cholera  and 
swine-plague  bacteria.  Bulletin  No.  6,  Bureau  of  Animal  Industry, 
U.  S.  Dept.  of  Agriculture,  1894,  p.  65. 

11.  Welch  and  Clements.  Remarks  on  hog  cholera  and  swine 
plague.     First  International  Congress  of  America.     Chicago.     1893. 


94  HEMORRHAGIC    SEPTICEMIA 

HEMORRHAGIC  SEPTICEMIA  IN  CATTLE. 

Synonyms.  Wild  zind  Rinderseuche;  Pasteurellosis  bovuni; 
Septicemie  hemorrliagique  du  boeuf. 

§  77.  Characterization.  Hemorrhagic  septicemia  in 
cattle  is  determined  b}'  an  acute  attack  usually  running  a 
rapid  course  and  terminating  fatally.  The  lesions  consist 
largely  of  hemorrhagic  areas  more  or  less  widely  distributed 
throughout  the  body  and  due  to  the  presence  ot  a  specific 
microorganism. 

§  78.  History.  In  1878,  Bollinger  described  under  the 
name  of  Wild  und  Rinderseuche  an  epizootic  disease  which 
killed  a  large  number  of  wild  boars  and  deer  in  the  Royal 
game  preserves  of  Munich.  After  the  disease  in  these  animals 
had  died  out,  the  domestic  cattle  in  the  neighborhood  began 
to  die  of  the  same  or  a  ver)^  similar  affection.  He  reports  it  to 
be  sudden  in  its  onset  and  rapidly  fatal  in  its  course,  with  a 
mortality  of  90  per  cent.  Death  occurred  in  from  12  hours  to 
a  few  days  after  the  appearance  of  symptoms. 

An  exanthematous  and  a  pectoral  form  are  described.  In 
the  exanthematous  form  there  are  large  and  small  hemorrhages 
disseminated  throughout  the  muscles  and  viscera.  The  intes- 
tines exhibit  large  numbers  of  ecchj^motic  areas,  while  the 
submucous  tissue  is  infiltrated  with  a  serous  exudate.  Large 
hemorrhagic  tumors  infiltrated  with  serum  are  abundant  in 
the  subcutaneous  tissue,  often  extending  into  the  muscles.  The 
mucous  membranes  of  the  tongue,  larynx  and  phar5'nx,  and  the 
lymphatic  glands  of  these  regions,  are  swollen  and  infiltrated 
with  more  or  less  bloody  serum.  In  the  pectoral  form,  there  is 
a  hemorrhagic  lobular  pneumonia,  with  considerable  infiltra- 
tion into  the  interlobular  tissue  of  a  serofibrinous  exudate. 
The  pleura  is  infiltrated  and  inflamed  and  covered  with  a 
fibrinous  exudate.  The  pleural  cavities  contain  from  two  to 
twenty-five  litres  of  liquid.  At  the  same  time  there  exist  a 
certain  degree  of  hemorrhagic  enteritis  and  the  widely  dissem- 
inated hemorrhagic  lesions  common  to  the  preceding  form. 


HISTORY 


95 


In  1885,  Kitt  studied  an  epizootic  disease  in  cattle  and 
swine  in  Sincbach.  From  this  disease  he  isolated  a  short, 
polar  staining,  non-motile,  rod-shaped  organism,  fatal  to  cattle, 
horses,  pigs,  sheep,  goats,  dogs  and  rabbits.  In  the  following 
year  Oreste  and  Armanni  reported  a  destructive  disease  of 
young  buffaloes  in  Italy  with  symptoms  and  lesions  similar  to 
those  reported  by  Bollinger  and  Kitt.  This  disease  had  been 
known  in  Italy  for  a  century  or  more,  where  in  certain  dis- 
tricts it  is  reported  to  have  recurred  with  great  regularity, 
destroying  both  old  and  young  animals.  In  the  same  year 
(1885)  Poels  described  a  septic  pleuro-pneumonia  in  calves 
which  prevailed  in  the  vicinity  of  Rotterdam.  It  was  of  a 
septicemic  nature.  From  the  organs  he  obtained  an  organism 
belonging  to  the  Bacillus  septicemiae  hcmorrhagicae  group  of 
bacteria.  In  1889,  Jensen  described  a  similar  disease  affecting 
calves  in  Jutland.  In  the  same  year  Piot  reported  the  presence 
of  "  barbone  "  in  the  buffaloes  and  domestic  cattle  in  Egypt. 
In  some  districts  40  per  cent,  of  the  horned  cattle  are  said  to 
have  died  in  a  single  year.  It  is  reported  as  being  more  preva- 
lent in  the  wet  season. 

In  1890,  Van  Ecke  described  a  hemorrhagic  septicemia 
in  cattle  in  Dutch  India,  particularly  in  Java,  the  lesions  of 
which  were  similar  to  those  first  described  by  Bollinger.  The 
specific  organism  was  virulent  for  rabbits,  mice,  turtle  doves, 
calves,  horses  and  swine ;  sheep  and  asses  were  almost 
immune.  In  the  following  year  Galtier  described  the  same 
disease  imported  from  Algiers  to  Lyons.  A  number  of  other 
investigators  have  studied  and  reported  cases  of  this  disease. 
In  1890,  Nocard  isolated  from  cases  of  broncho-pneumonia  in 
American  cattle  landed  at  La  Villette,  France,  an  organism 
similar  to  that  described  as  the  cause  of  septicemia  hemor- 
rhagica. In  1896,  Smith  called  attention  to  a  similar  organism 
which  he  found  in  cases  of  sporadic  pneumonia  in  cattle  ;  he 
does  not  think,  however,  that  this  organism  was  primarily  the 
cause  of  the  disease,  giving  it  a  secondary  place  in  the  eti- 
ology. As  early  as  1891,  Smith  published  the  discovery  of  the 
presence  of  an  organism  morphologically  and  in  its  cultural 


96  HEMORRHAGIC    SEPTICEMIA 

characters  identical  with  that  of  swine  plague  in  the  upper  air 
passages  of  healthy  swine.  The  same  year  Moore  reported  the 
presence  of  a  like  organism  in  the  upper  air  passages  of  cattle, 
horses,  sheep,  dogs  and  cats.  The  following  year.  Fiocca  de- 
scribed a  pathogenic  bacterium  resembling  that  of  rabbit  septi- 
cemia in  the  saliva  of  healthy  cats  and  dogs. 

Hueppe  proposed  the  name  Bacillus  septicemiae  henior- 
rhagicae  for  this  group  of  organisms  and  septicemia  hemor- 
rhagica for  the  disease  they  produce.  Lignieres  has  designated 
the  diseases  caused  by  this  group  as  Pasteurelloses.  While 
there  may  be  objections  to  this  unifying  name,  there  seems  to 
be  no  serious  reason  for  not  accepting  it  as  a  working  hypoth- 
esis. In  1898,  Fennimore  described  under  the  name  of  "Wild 
and  Cattle  Disease  "  a  malady  occurring  in  Eastern  Tennessee. 
Its  serious  nature  caused  an  investigation  to  be  made  by  the 
Tennessee  Agricultural  Experiment  Station.  Norgaard,  who 
assisted  in  this  investigation,  recognized  it  as  the  same  disease 
as  that  described  by  Bollinger  in  1878.  Fennimore  states 
that  it  has  occurred  to  a  considerable  extent  in  his  practice. 
In  1 901,  it  was  carefully  studied  by  Wilson  and  Brimhall  for 
the  Minnesota  State  Board  of  Health.  They  report  64  cases 
of  this  affection  which  they  have  examined  in  cattle  in  the 
state  of  Minnesota.  In  1903,  Reynolds  described  an  investi- 
gation into  several  outbreaks  of  this  disease  in  the  same  state. 
It  is  from  the  two  latter  reports  that  we  draw  very  largely  for 
the  symptoms  and  morbid  anatomy  of  this  disease  in  cattle. 

§  79.  Geographical  distribution.  It  will  be  seen  from 
the  history  that  this  disease  is  a  wide  .spread  malady  occurring 
in  nearly  every  country.  It  appears  to  be  quite  prevalent  in 
the  western  and  northern  parts  of  the  Mississippi  valley. 
It  occurs  in  other  localities  more  rarely. 

§  80.  Etiology.  Septicemia  hemorrhagica  in  cattle  is 
caused  by  an  organism  belonging  to  the  group  of  bacteria 
designated  by  Hueppe  as  the  hemorrhagic  septicemia  group 
and  specifically  named  Bacillus  boviseplicjis  by  Kruse.  This, 
according   to    Migula's   classification,    should    be    Bacterium 


SYMPTOMS  97 

bovisepticuvi.     A  brief  description  of  the  organism  as  given  by 
Wilson  and  Brimhall  is  appended. 

"The  organism  has  a  strong  tendenc}'  to  show  polar  staining  in  tis- 
sues and  to  form  chains  of  much  shortened  individuals  in  liquid  media, 
which  causes  it  to  be  mistaken  in  examinations  of  a  single  specimen  for 
a  (liplococcusora  streptococcus.  Sometimes  in  cover-glass  preparation^ 
from  solid  organs  and  very  frequently  in  those  from  body  fluids  and 
liquid  cultures,  the  bacteria  were  found  in  chains  of  three  to  twelve 
individuals.  In  cover-glass  preparations  the  bacteria  are  from  0.6/7  to 
0.8//  broad  and  from  i.o  to  1.5//  in  length.  In  tissues  which  have  been 
fixed  in  96  per  cent,  alcohol,  they  are  somewhat  smaller.  In  cultures, 
especially  in  fluid  media,  they  are  apt  to  be  much  smaller  and  approach 
diplococci  in  appearance.  The  ends  are  rounded.  In  stained  prepara- 
tions directly  from  the  tissues  most  of  the  bacteria  have  the  ends 
intensely  stained  and  the  central  portion  but  faintly  so.  In  some  chains 
in  rapidly  growing  broth  cultures  this  is  not  the  case,  many  of  the  indi- 
vidual bacteria  being  evenly  stained  throughout  and  somewhat  pointed 
at  the  ends.  They  do  not  retain  the  stain  by  Gram's  method.  The 
organism  is  non-motile.  It  is  aerobic,  but  prefers  the  depths  rather 
than  the  surfaces  of  the  media.  It  grows  best  at  the  body  temperature 
and  more  slowly  at  room  temperature.  In  plain  and  dextrose  broth  a 
growth  appears  in  24  hours.  In  Dunham's  solution  a  small  amount  of 
indol  is  formed  in  4S  hours.  No  coagulation  of  milk.  On  Liiffler's 
blood  serum,  direct  from  the  diseased  tissues,  it  failed  to  grow  well.  On 
potato  no  appreciable  growth  has  been  obtained.  In  gelatin  plates 
small,  granular,  white  to  slightly  yello%vish  colonies  appear  after  48 
hours.  In  gelatin  stab  cultures  a  light  growth  occurs  on  the  surface, 
while  along  the  needle  tract  numerous  colonies  like  those  in  the  deep 
portions  of  the  plate  cultures  develop.  The  bacteria  are  destroyed  in 
fluids  at  58°  C.  in  7  or  8  minutes,  by  i  to  5,000  mercuric  chloride  in  one 
minute,  and  by  a  solution  of  lime  water  as  weak  as  0.04  per  cent, 
almost  immediately." 

The  period  of  incubation  is  supposed  to  be  very  short. 
The  method  of  infection  is  not  known. 

§  81.  Symptoms.  There  is  little  opportunity  to  deter- 
mine the  symptoms.  The  animals  observed  at  the  onset  of  the 
disease  by  Wilson  and  Brimhall  appeared  to  be  dumpish  and 
out  of  sorts.  There  is  sudden  stopping  of  the  milk  secretion  in 
milch  cows.  As  a  rule  the  affected  animals  refuse  food.  Of 
the  few  that  make  an  attempt  to  eat,  those  with  affected  throats 
are  unable  to  swallow    except   with    much    difficulty.      These 


98  HEMORRHAGIC     SEPTICEMIA 

cases  also  breathe  ver)'  heavily.  The  animals  show  marked 
disinclination  to  move  and  when  incited  to  do  so,  exhibit  stiff- 
ness, and  in  some  instances  actual  lameness.  Animals  have 
been  observed  to  drop  to  the  ground  and  die  in  a  short  time, 
apparently  without  pain.  Other  animals  live  for  several  hours 
in  great  pain  as  indicated  by  groans  and  spasms  of  the  muscles. 
The  paroxysms  of  pain  are  apparently  intermittent.  There  is 
extremely  rapid  loss  of  flesh  in  the  animals  that  are  sick  for 
any  length  of  time. 

Reynolds  has  observed  the  symptoms  in  a  few  cases.  He 
describes  three  .stages.  First  (24-36  hours)  general  dullness 
and  checking  of  milk  secretion.  Second,  diarrheal  discharge 
dark  in  color,  and  of  disagreeable  odor.  The  breath  was 
noticed  to  be  offensive.  In  some  cases  nervous  symptoms 
developed.  The  temperature  remained  about  normal  during 
this  period.  Third,  in  this  stage  the  eyes  are  wild,  there  is 
grinding  of  the  jaws,  convulsions  of  the  face  and  neck  muscles 
followed  by  a  period  of  intense  restlessness  and  activity. 

He  also  records  the  observation  that  the  cases  that  ap- 
peared to  be  the  worst  in  the  beginning  lived  longer  than 
those  that  appeared  to  be  mild. 

Opportunities  for  the  accurate  determination  of  tempera- 
ture at  the  beginning  of  the  disease  have  been  very  few.  An 
initial  temperature  of  105.6°  F.  followed  by  a  rapid  decline 
has  been  observed.  Painful  edematous  swellings  about  the 
legs,  shoulders  and  under  the  throat  are  noted  as  early  symp- 
toms. The  intestinal  discharges  are  often  streaked  with 
blood.  In  other  cases  the  feces  are  black,  tarry  or  of  a  bloody, 
serous  nature.  Bloody  urine  and  a  bloody  serous  discharge 
from  the  nose  have  been  present  in  some  cases.  The  vaginal 
and  rectal  mucous  membranes  are  intensely  congested. 

The  marked  sweUing  of  the  face,  stomatitis,  glossitis,  and 
convulsive  movements  of  the  jaws  in  the  pneumonic  form  of 
the  disease,  described  by  European  writers,  more  especially 
Bollinger,  were  not  observed  by  Wilson  and  Brimhall  or  by 
Reynolds. 


MORBID    ANATOMY  99 

The  duration  of  the  disease  is  short.  Often  the  animals 
are  found  dead. 

The  prognosis  is  unfavorable.  The  mortality  is  placed  at 
from  80  to  90  per  cent  of  the  animals  affected. 

^  82.  Morbid  anatomy.  The  characteristic  lesions  of 
the  disease  are  widely  distributed  areas  of  hemorrhage,  vary- 
ing in  size  from  a  pin  point  to  several  centimeters  in  diameter. 
They  vary  in  color  from  light  red  to  almost  black.  They  are 
frequently  accompanied  with  a  sero-fibrinous  exudate,  u.sually 
yellow,  but  occasionally  dark  red  in  color.  The  hemorrhagic 
areas  in  the  animals  just  dead  are  not  so  dark  as  those  in 
animals  that  have  been  dead  for  some  hours.  The  large  areas, 
some  centimeters  in  diameter,  are  apparently  due,  in  some 
instances  at  least,  to  single  hemorrhages,  infiltrating  an  exten- 
sive mass  of  tissue,  and  in  others  to  a  number  of  minute  hem- 
orrhages closely  placed  and  partially  coalescing.  Gas  is  not 
present  in  the  subcutaneous  connective  tissue  except  in  cases 
where  extensive  post-mortem  changes  have  occurred. 

There  is  extensive  fullness  of  the  vessels  of  the  subcu- 
taneous connective  tissue  in  the  acute  cases,  especially  in 
those  animals  which  are  not  killed  by  bleeding.  In  animals 
which  live  until  emaciation  is  marked,  there  is  no  engorgement 
of  the  vessels. 

Reynolds  reports  one  outbreak  in  which  meningitis 
involving  the  spinal  cord,  brain  or  both  of  these  organs  were 
invariably  present. 

All  cases  show  some  hemorrhagic  areas  in  the  subcutane- 
ous tissue,  though  the  number  and  size  of  these  vary  greatly 
in  the  different  cases.  Some  animals  show  not  over  a  dozen 
areas  between  two  and  three  centimeters  in  diameter,  though 
many  minute  ones  are  present.  In  other  animals,  on  remov- 
ing the  skin,  hemorrhagic  areas  are  found  in  great  numbers 
and  so  extensive  that  a  large  fraction,  possibly  one-eighth, 
of  the  body  surface  appears  to  be  involved.  The  large  hemor- 
rhages in  the  subcutaneous  connective  tissue  appear  to  be  of 
the  composite  type  noted  above. 


HEMORRHAGIC     SEPTICEMIA 


The  location  of  the  superficial  lesions  varies  in  different 
animals.  In  most  cases  the  parts  about  the  shoulder  are  most 
affected.  A  few  animals  show  marked  lesions  in  the  gluteal 
and  inguinal  regions. 

At  first  sight  the  muscle  tissue  in  some  cases  seems  to  be 


Fig.   14.     Photograph  sho~iOing  hcDiorrhages  beneath  the  eiidocardiu-tn 
of  the  right , ventricle  (Reynolds). 

much    involved.      A    closer    examination,    however,     usually 
shows  that  while  some  of  the  minute  hemorrhages  are  in  the 


MORHin    ANATOMY  lOI 

muscle  proper,  the  larger  ones  are  in  the  intermuscular  con- 
nective tissue.  They  are  usualh'  accompanied  by  a  consider- 
able quantity  of  yellowish  or  blood-stained  serous  exudate. 
The  intermuscular  connective  tissue  appears  to  be  quite  as 
much  involved  as  the  subcutaneous  connective  tissues. 

The  lymphatic  glands  are  frequently  though  not  uniformly 
nor  constantly  enlarged.  Those  that  are  enlarged  are  edema- 
tous and  often  hemorrhagic.  The  cervical  and  prescapular 
glands  are  most  seriously  affected. 

The  nasal  mucous  membrane  in  some  cases  is  congested, 
and  a  bloody  serous  discharge  from  the  nostrils  is  present. 
The  tissues  around  the  larynx  are  hemorrhagic  and  infiltrated 
with  blood-stained  serum.  The  mucous  membranes  of  the 
larynx  and  trachea  are  more  or  less  congested  and  covered 
with  a  frothy  mucus,  sometimes  streaked  with  blood.  In  some 
instances  no  lesions  are  observable  in  these  organs.  The  lungs 
are  in  general  almost  fere  from  evidence  of  disease.  Occasion- 
ally there  are  a  small  number  of  hemorrhagic  areas,  pyramidal 
in  shape  with  their  base  on  the  pleura.  In  most  cattle  the 
parietal  pleura  is  studded  with  small  hemorrhages.  The 
diaphragm  sometimes  contains  very  large  hemorrhagic  areas. 

The  pericardial  sac  usually  shows  small,  sometimes  very 
numerous,  hemorrhages  in  the  walls,  and  in  man^v  instances 
contains  a  blood-stained  serum. 

The  heart  walls,  with  but  few  exceptions,  contain  ecchy- 
moses  and  petechiae.  These  sometimes  extend  deep  into  the 
muscle.  Similar  areas  of  hemorrhage  are  also  visible  in  the 
endocardium.  The  heart  usually  contains  post-mortem  blood 
clots. 

The  blood,  in  animals  just  dead,  is  said  to  be  somewhat 
lighter  than  normal  in  color.  When  post-mortem  changes 
set  in,  the  blood  is  darker  in  color,  but  reddens  on  exposure 
to  the  air. 

The  spleen  shows  on  its  surface  a  few  small  hemorrhagic 
areas.  It  is  usually  normal  in  size,  color  and  consistency, 
except  where  post-mortem  changes  have  taken  place. 


I02  HEMORRHAGIC    SEPTICEMIA 

Stomatitis  and  glossitis  are  rarely  observed.  The  pharynx 
is  usually  congested. 

The  stomach  walls  contain  a  few  or  many  hemorrhagic 
areas.  These  are  sometimes  extremely  large,  especially  on 
the  third  stomach.  As  a  rule  the  larger  hemorrhages  pene- 
trate the  entire  thickness  of  the  walls  The  smaller  ones  are 
confined  to  the  subserous  or  mucous  coats.  The  stomach  con- 
tents are  apparently  normal. 

The  intestinal  walls  are  constantly  affected.  Hemorrhagic 
areas  involving  all  the  coats  are  frequently  present.  Smaller 
ones,  visible  only  from  the  inner  or  outer  surface,  are  always 
present.  General  enteritis  and  peritonitis  are  constantly 
observed.      lyOcalized  enteritis  is  frequent. 

The  bowel  contents  are  in  some  cases  dark  and  tarry  :  in 
others  the  feces  are  apparently  normal  in  color  and  consistency 
but  streaked  with  bloody  mucous. 

The  kidneys  are  usually  but  slightly  affected.  When 
lesions  are  present  they  are  hemorrhages  but  pin  point  in  size 
and  mostly  confined  to  the  cortical  substance,  though  a  few 
are  found  in  the  walls  of  the  pelvis  and  ureters.  The  urine  is 
bloody  in  some  instances. 

The  vaginal  mucous  membrane  is  congested  in  many 
cases.  Wilson  and  Brimhall  saw  one  animal  that  was  four 
months  pregnant  which  exhibited  small  hemorrhagic  areas  in 
the  placental  membranes. 

The  udder  is  congested  in  some  cases.  It  may  be 
hemorrhagic. 

The  central  nervous  system  occasionally  shows  hemor- 
rhages in  the  dura.  A  few  cases  are  reported  of  hemorrhages 
on  all  of  the  joint  surfaces.  Brimhall  recently  reported  an 
outbreak  where  the  autopsies  showed  very  few  hemorrhagic 
areas  in  the  subcutis  and  internal  organs.  There  were  lesions 
in  its  spinal  cord.  The  spleens  were  enlarged.  In  nine  out- 
breaks Bad.  boviscptiaiyn  was  present. 

Wilson  and  Brimhall  fixed  portions  of  the  subcutaneous 
tissue,  skeletal  muscles,  lymphatic  glands,  lung,  heart  wall, 
stomach  wall,  and  spleen  in  95  per  cent,  alcohol  and  in  4  per 


DIFFERENTIAL    DIAGNOSIS  IO3 

cent  formaldehyde  solution  and  stained  by  various  methods. 
In  general  the  lesions  found  were  enormous  extravasations  of 
blood,  some  recent  and  some  showing  coagulation  of  fibrin. 
In  the  areas  of  less  recent  hemorrhage,  the  surrounding  tissues 
showed  varying  degrees  of  ordinary  coagulation  necrosis. 
This  was  particularly  marked  in  the  affected  muscles,  lymph 
glands  and  portions  of  the  lungs.  In  the  borders  of  such 
necrosed  areas  leucocytic  infiltration  was  not  infrequent.  In 
the  spleen,  in  which  the  hemorrhagic  areas  were  neither  num- 
erous nor  large,  there  was  in  some  instances  an  apparent 
destruction  or  shrinkage  of  the  parenchyma. 

A  very  important  feature  in  this  disease  has  been  brought 
out,  namely,  that  it  is  necessary,  in  order  to  obtain  cultures  of 
the  bacterium  producing  it,  that  the  media  should  be  inocu- 
lated at  once.  It  is  evident  from  the  literature,  that  with  this 
precaution  cultures  should  invariably  be  obtained. 

§  83.  Differential  diagnosis.  Septicemia  hemorrhagica 
in  cattle  must  be  differentiated  from  anthrax,  symptomatic 
anthrax,  and  the  affection  known  as  "corn-stalk  disease." 
Death  from  this  disease  must  also  be  distinguished  from  those 
due  to  certain  accidental  causes,  poisoning,  or  the  effect  of 
over  eating  of  grain  or  green  fodder  (hoven).  The  sudden- 
ness with  which  the  animals  may  die  from  all  of  these  causes 
renders  the  symptoms,  should  they  be  observed,  of  very  little 
value  in  making  a  diagnosis.  It  is  necessary,  therefore,  that 
in  all  cases,  especially  with  the  first  animals  to  die,  careful 
post-mortem  and  bacteriological  examinations  should  be  made. 

In  case  of  septicemia  hemorrhagica,  the  cultures  will 
usually  reveal  the  presence  oi  Bad.  boviscptiaim.  The  le.sions 
will  be  hemorrhagic  in  nature. 

In  case  of  the  "cornstalk  disease  "  the  lesions  may  consist 
of  small  hemorrhages  (petechias)  especially  of  the  serous  mem- 
branes and  heart.     The  cultures  will  be  negative. 

With  anthrax  and  symptomatic  anthrax,  their  specific 
bacteria  will  be  found. 

^  84.      Prevention.     When   this  di.sease  occurs  it  is  im- 


I04  HEMORRHAGIC     SEPTICEMIA 

portant  to  remove  the  unaifected  animals  to  other  fields  or 
enclosures.  It  is  well  to  divide  them  into  small  groups  if 
possible.  The  carcasses  of  animals  that  die  should  be  burned 
or  buried  deeply  with  a  good  covering  of  a  disinfectant,  such 
for  example,  as  quick  lime.  Should  death  occur  in  a  stable, 
all  contaminated  litter  should  be  burned  and  the  floors,  man- 
gers and  walls  thoroughly  disinfected. 

Experiments  directed  towards  protective  inoculation  have 
been  made,  but  thus  far  the  results  have  not  been  sufficiently 
satisfactory  to  warrant  the  recommendation  of  the  methods. 

REFERENCES. 

1.  Bollinger.  Ueber  eine  neue  Wild  und  Rinderseuche. 
IVIiinchen.     1878. 

2.  Brimhall.  Haemorrhagic  septicemia  in  cattle.  A)ne>-.  Vet. 
Rev.,  Vol.  XXVII  I  1903-4),  p.  103. 

3.  Fennimore.  Wild  and  cattle  disease.  Jonr.  of  Comp.  Med. 
ami  Vet.  Arcliiv.,  Vol.  XIX  ^l89S),  p.  625. 

4.  Galtier.  Nouveaux  faits  tendant  a  etablir  que  la  pneumo- 
enterite  infectieuse  existe  sur  les  grands  et  les  petits  ruminants  en 
algerie.     Rectieil  de  Med.   Vet..  7  serie,  Vol.  VIII  (1891 ),  p.  97. 

5.  HuEPPE.  Ueber  die  Wildseuche.  Berlin  klinisclie  Wocfieii- 
sc/iri/i,  18S6,  S.  753. 

6.  KiTT.  Ueber  eine  Experimentelle,derRinderseuche(Bollinger) 
ahnliche  Infectionskrankheit.  Sitzungsberic/ite  der  Geseilscliaft  fiir 
Morphologic  und  Physiologie  in  Miinehen,  I.     1885,  S.  240. 

7.  PioT.  Le  Barbone  du  Ruffle.  Bulletin  d  V Instut.  Egyptien, 
1889. 

8.  PoELS.  Septische  Pleuropneumonie  der  Kalber.  Fortschr.  d. 
Med.,  1S86,  S.  388. 

9.  Reynolds.  Htemorrhagic  Septicaemia.  Am.  Vet.  Review. 
Vol.  XXVI  (1902),  p.  819. 

10.  Reynolds.  Htemorrhagic  Septicaemia.  Bulletin  No.  S2,  Minn. 
Agric.  Experiment  Station,  1903. 

If.  Wilson  and  Brimhall.  Sixty-four  cases  of  hemorrhagic 
septicemia  in  cattle  due  to  bacillus  bovisepticus.  Report  .State  Board 
0/ Health  0/ Minnesota,  i<^oi.     (Very  full  bibliography,  i 

12.  WooLSEV  .\ND  Job  LING.  A  report  on  hemorrhagic  septicemia 
in  animals  in  the  Philippine  Islands.  1903.  No.  9.  Bureau  of  Gov- 
ern>nent  Laboratories,  Manila,  P.  I. 


FOWL    CHOLERA  IO5 

FOWI<  CHOLERA. 

Synonyms.  Chicken  cholera;  cholera  gallhiarmn;  Hi/lmer 
cholera:  Pastcurellosis  avium;  cholera  dcs  ponies. 

%  85.  Characterization.  This  is  au  infectious  disease 
of  fowls  caused  by  bacteria,  and  transmissable  by  cohabitation 
and  inoculation.  It  is  determined  by  a  high  fever,  great  weak- 
ness and  prostration,  and  usually  terminates  in  the  death  of 
the  affected  bird.  It  is  reported  that  it  attacks  all  varieties  of 
domesticated  poultry  (chickens,  ducks,  geese,  pigeons,  tur- 
keys), and  caged  birds  such  as  parrots  and  canaries.  It  also 
attacks  some  species  of  wild  birds.  It  is  communicable  by 
inoculation  to  rabbits  and  mice.  Guinea  pigs  are  not  very 
susceptible. 

i^  86.  History.  This  disease  is  mentioned  in  some  of 
the  oldest  works  treating  of  the  diseases  of  animals.  Fowl 
cholera  was  studied  b}^  Chabert  in  1782,  who  regarded  it  as  a 
form  of  anthrax.  Since  1825,  it  has  been  frequently  observed 
in  France  where  it  caused  enormous  losses  in  1830,  in  1850  and 
in  i860.  About  1830,  it  became  known  in  Russia,  Bohemia 
and  Austria.  In  1851,  Benjamin  considered  it  to  be  a  con- 
tagious disease  but  remarked  that  people  and  dogs  might  con- 
sume with  impunity  the  meat  of  affected  fowls.  Delafond 
observed  that  it  might  be  transmitted  to  birds  and  rabbits  by 
using  blood,  secretions,  and  portions  of  the  flesh.  It  was  also 
recognized  that  the  excrement  plays  an  important  part  in  the 
dissemination  of  the  virus. 

During  recent  years  it  has  been  observed  in  nearly  all  of 
the  countries  of  Europe  as  well  as  in  the  United  States.  It 
has  been  reported  from  many  places  in  the  United  States,  but 
its  presence  seems  to  have  been  determined  by  scientific 
investigation  in  but  a  very  few  of  these.  Salmon  investigated 
it  in  South  Carolina  in  1879-80,  and  Higgins  in  1898  reported 
it  from  Canada.  Salmon  gave  special  attention  to  vaccination 
and  the  effect  of  disinfectants  in  destroying  the  virus.  In 
1904,  Ward  reported  an  outbreak  in  California. 


I06  FOWL    CHOLERA 

Perroncito  was  among  the  first  to  describe  the  specific 
cause  of  the  disease.  This  was  followed  by  the  contributions 
of  Pasteur,  who,  in  1880,  cultivated  the  bacterium  in  chicken 
broth  and  showed  that  its  virulence  might  be  reduced  to  such 
an  extent  that  it  could  safely  be  used  for  vaccination.  This 
is  the  first  case  in  which  a  virulent  organism  was  successfully 
modified  in  a  laboratory  and  made  to  act  as  a  vaccine.  It  was 
the  forerunner  of  the  preparation  of  vaccines  for  a  number  of 
diseases,  more  particularly  for  anthrax,  black  quarter,  and 
rabies. 

§  87.  Geographical  distribution.  Fowl  cholera  seems 
to  be  widely  distributed  in  Europe  and  it  has  been  found  in  a 
few  localities  in  the  United  States  and  in  Canada.  In  Ger- 
many it  is  the  cause  of  heavy  losses  among  poultry.  In  1903 
it  is  reported  to  have  killed  over  48,000  fowls  and  23,000  geese 
besides  other  poultry. 

§  88.  Etiology.  Fowl  cholera  is  caused  by  a  specific 
bacterium  {Bacillus  {bipolaris)  avisepticus,  Pasteurella  avium^ 
which  is  not  distinguishable  morphologically  or  in  its  cultural 
manifestations  from  the  other  members  of  the  group  of  bacteria 
of  which  Bad.  septicemiae  hemorrhagicae  is  the  type.  In  this 
group  are  the  bacteria  of  rabbit  septicemia,  swine  plague,  and 
Wildseicche.  It  is  a  small,  slightly  elongated  organism  with 
rounded  ends.  In  stained  preparations  from  the  tissues  it 
exhibits  a  pronounced  polar  stain. 

The  period  of  incubalion  is  placed  by  European  writers  at 
from  18  to  48  hours.  In  the  case  of  40  fowls  inoculated  by 
Salmon,  it  varied  from  4  to  20  days,  the  average  period  being 
8  days.  Ward  fed  viscera  of  dead  fowls  to  10  healthy  ones. 
They  died  in  from  24  hours  to  6  days. 

§  89.  Symptoms.  The  symptoms  described  for  this 
disease  in  Europe  differ  somewhat  from  those  reported  by 
Salmon.  Usually  the  appetite  is  lessened.  Occasionally  they 
continue  to  eat  almost  to  the  time  of  death.  The  earliest  indi- 
cation of  the  disease  is  a  yellow  coloration  of  the  urates.     In 


MORBID      ANATOMY  IO7 

health,  these  are  a  pure  white  though  they  are  frequently 
tinted  with  yellow  as  the  result  of  disorders  other  than  cholera. 

Occasionally  the  first  symptom  is  a  diarrhea  in  which  the 
excrement  is  passed  in  large  quantities  and  consists  almost 
entirely  of  white  urates  mixed  with  colorless  mucus. 

Very  soon  after  the  first  symptoms  appear  the  bird  sepa- 
rates itself  from  the  flock,  it  no  longer  stands  erect,  the 
feathers  are  roughened,  the  wings  droop,  the  head  is  drawn 
down  towards  the  body  and  the  general  outline  of  the  bird 
becomes  spherical  or  ball-shaped.  At  this  period  there  is 
great  weakness,  the  affected  bird  becomes  drowsy  and  may 
sink  into  a  sleep  which  lasts  during  the  last  daj-  or  two  of  its 
life,  and  from  which  it  is  almost  impossible  to  arouse  it. 

The  crop  is  nearly  always  distended  with  food  and  appar- 
ently paralyzed.  There  is  in  most  cases  intense  thirst.  If 
the  birds  are  aroused  and  caused  to  walk,  there  is  at  first  an 
abundent  discharge  of  excrement  followed  at  short  intervals 
by  scanty  evacuation. 

With  the  beginning  of  diarrhea  the  body  temperature 
rises  to  109  to  rio°  F.  Ward  states  that  in  advanced  stages  it 
ranges  from  109  to  112°  F.  The  comb  loses  its  bright  hue 
and  becomes  pale  and  bloodless.  European  writers  describe 
the  comb  as  dark  blue,  purple,  or  black,  and  some  writers  in 
the  United  States  have  referred  to  it  in  the  same  terms.  Sal- 
mon reports  that  he  never  observed  it. 

Di.seased  birds  rapidly  lose  in  weight.  They  become  so 
weak  that  they  walk  with  great  difficulty,  a  slight  touch  causes 
them  to  fall  over.  The  fowls  become  very  much  emaciated. 
Death  may  occur  without  a  struggle  or  there  may  be  convul- 
sive movements  and  cries. 

This  disease  may  run  rapidly  through  a  flock  destroying 
the  greater  part  of  the  birds  in  a  week,  or  it  may  assume  a 
more  chronic  form,  spreading  slowly,  and  remain  upon  the 
premises  for  several  weeks  or  months. 

i^;  90.  Morbid  anatomy.  The  comb  is  pale  and  blood- 
less. The  superficial  blood  vessels  usually  contain  but  little 
blood. 


I08  FOWL    CHOLERA 

The  liver  is  usually  enormously  enlarged,  softened,  and 
the  blood  vessels  are  engorged.  The  gall  bladder  is  distended 
with  thick,  dark  bile. 

The  crop  is  usually  distended  with  food.  The  stomach 
often  presents  externally  a  number  of  circular  discolorations, 
about  three  millimeters  in  diameter,  which  on  section  are 
found  to  be  extravasated  blood.  The  small  intestines  are 
congested. 

The  rectum  and  cloaca  usually  present  deep,  red  lines 
upon  their  mucous  membrane,  evidently  the  first  stage  of 
inflammation,  which  results,  in  chronic  cases,  in  thickening  of 
the  walls,  especially  of  the  rectum,  the  desquamation  of  the 
mucous  membrane  and  the  formation  of  large  ulcerated 
surfaces. 

The  mesenter}'  is  generally  congested,  often  greatly 
thickened  and  reddened,  and  rendered  opaque  by  inflamma- 
tion. The  ureters  are  distended  with  yellow  urates ;  the 
kidneys  seem  engorged,  and  on  section  accumulations  of  the 
tenacious,  yellow  urates  are  frequently  seen.  The  spleen  is 
generally  normal  in  size  and  appearance,  though  frequently 
enlarged  and  softened. 

The  pericardium  is  sometimes  distended  with  effusions,  in 
which  case  there  is  noticeable  hyperemia  of  the  surface  of  the 
heart.  The  lungs  are  often,  though  not  generally,  engorged 
with  dark  blood  ;  they  are  seldom,  if  ever,  hepatized. 

The  blood  vessels  are  sometimes  filled  with  a  firm  clot, 
and  contain  but  little  liquid  ;  at  other  times  the  blood  does 
not  coagulate  at  all.  It  seems  to  be  those  cases  in  which  the 
duration  of  the  disease  is  the  longest,  that  the  blood  loses  its 
power  to  coagulate. 

Ward  has  summarized  the  morbid  anatomy  in  the  fowls 
examined  by  him  as  follows  : 

"  At  death,  or  some  hours  previous,  the  comb  frequently  takes  on  a 
dark  purple  color,  but  this  does  not  always  occur.  Very  often  the  comb 
is  pale  and  bloodless.  The  skin  of  the  breast  and  abdomen  is  frequently 
reddened. 

"  In  post-mortem  examinations  a  congestion  of  the  blood  vessels  of 
the  liver,  kidney,  mesentery,  or  intestines  is  noticeable  to  some  degree 


MOKHII)    ANATOMY  IO9 

in  all  cases  Punctiform  hemorrhages  are  found  upon  the  heart  with 
almost  absolute  uniformity.  The  liver  is  very  fre(|uently  marked  with 
punctiform  whitish  areas  of  necrosis.  Stained  sections  show  these 
necrotic  foci  throughout  the  substance  of  the  liver,  and  besides  reveal  a 
congestion  of  the  blood  vessels  of  that  organ.  The  next  most  striking 
lesions  occur  in  the  first  and  second  duodenal  flexures.  The  mucosa  is 
deeply  reddened  and  studded  with  hemorrhages  varying  in  size,  but 
seldom  exceeding  one  millimeter  in  diameter.  These  involve  the 
intestinal  coats  to  an  extent  that  makes  them  distinctly  visible  on  the 
peritoneal  surface.  The  contents  of  the  duodenum  consist  of  a  pasty 
mass,  more  or  less  thickly  intermingled  with  blood  clots.  The  intes- 
tinal contents  sometimes  consist  of  a  cream-colored  pasty  mass,  or  may 
be  brownish  red  or  even  green  in  color.  Lesions  are  very  rarely 
observed  in  other  portions  of  the  intestines.  The  ureters  are  noticeable 
in  practically  all  cases  by  reason  of  the  yellow-colored  urates  that  they 
contain.  The  nasal  cavity,  pharynx  and  oral  cavity  frequently  contain 
a  viscous  mucous  fluid,  probably  regurgitated  from  the  crop. 

"  The  field  notes  on  twenty-one  post-mortem  examinations  refer  to 
hemorrhages  in  the  heart  in  twenty-one  cases  ;  punctiform  necroses  in 
the  liver,  fifteen  cases  ;  hemorrhages  in  duodenum,  seven  cases  ;  the 
discoloration  of  the  skin  in  six  cases.  The  presence  of  a  gelatinous 
exudate  within  the  pericardium  was  noted  twice.  A  fibrinous  exudate 
in  the  pericardium  occurred  the  same  number  of  times.  Hemorrhages 
in  the  peritoneum  other  than  those  visible  through  the  mucosa  of  the 
duodenum  occurred  but  twice.  In  one  case  hemorrhages  were  abund- 
antly scattered  tliroughout  the  muscles  of  the  trunk  and  legs. 

"  Fowls  inoculated  subcutaneously  with  cultures  exhibit  on  post- 
mortem examination  the  punctiform  hemorrhages  on  the  heart  and  the 
hemorrhages  in  the  mucosa  of  the  duodenum  exactly  as  incases  infected 
naturally." 

BI^OOI)     COUNTS     0\-     FOWLS     INFECTKD     HV     INC,]-,STION     AND 
INFECTED     NATrRAl.I.V. 


;posure  to  infection 44.8'^  C. 

— -  43-7°  C. 

-—  43-3°  C. 

42.8°  C. 

....  42.2°  C. 

cted -  42.S°C. 


Fowl. 

White 

Red 

R. 

Corpuscles 

Covpuscle.s. 

No.  3 

23,000 

2.290  000  per  cnnn. 

3  days  al 

No.  3 

20,000 

2,Soo,ooo   ■'         " 

No.  6 

37,000 

3,930,000   " 

No.  8 

87,000 

4,490,000   •• 

No.  8 

101,000 

2,960,000   •'         •• 

A     -- 

.=i8.ooo 

1,710,000   " 

Natnrall 

B... 

4.S.000 

1.925,000   " 

FOWL    CHOLERA 
BLOOD     COUNTS     OF     APPARENTLY     HEALTHY     FOWLS. 


Red  Corpuscles. 

2,980,000  per  cmm. 

2,987 

000     " 

3.115 

000     " 

3.980 

000    " 

3,920 

000     "        " 

2,380 

000    " 

2,620 

000     " 

Fowl.  White  Corpuscle 

No.  II -  24,000 

No.   12.. 26,300 

No.  14 36-000 

No.  15 52,000 

No.  16 61,000 

No.  17 30,000 

No.  iS -_-  24,000 

The  duration  of  the  disease  varies  from  a  few  hours  to 
several  days. 

The  prognosis  is  unfavorable.  The  mortality  is  very  high, 
often  100  per  cent. 

§  91.  Differential  diagnosis.  Fowl  cholera  is  to  be 
differentiated  from  : 

1.  A  number  of  dietary  disorders  which  cause  the  death 
of  a  large  number  of  fowls.  Such  cases  are  often  thought  to 
be  chicken  cholera  and  so  reported  by  the  owners.  A  diagno- 
sis is  to  be  made  from  the  bacteriological  findings. 

2.  It  is  to  be  differentiated  from  fowl  typhoid.  There 
There  are  a  number  of  resemblances  in  the  clinical  history  of 
the  two  diseases  but  there  are  marked  differences  in  both  the 
morbid  anatomy  and  etiology.  For  a  comparison  of  the  lesions 
and  specific  bacteria  of  these  two  diseases  see  fowl  typhoid. 

§  92.  Prevention.  Pasteur  introduced  a  preventive 
inoculation  or  vaccine  for  this  disease.  Kitt  has  found  that 
the  eggs  of  fowls  unknown  to  this  disease  possessed  a  sub- 
stance somewhat  similar  to  antitoxin.  He  immunized  fowls 
by  injecting  them  simultaneously  with  from  four  to  eight 
cubic  centimeters  of  the  whites  of  such  eggs.  While  exceed- 
ingly interesting  this  method  does  not  seem  practicable.  More 
recently  he  has  obtained  a  horse  serum  that  promises  to  be  of 
immunizing  value.  Good  sanitary  conditions,  isolation  of  the 
well  from  the  sick  fowls  and  thorough  disinfection  seems  to 
be  the  most  satisfactory  procedure.  It  is  important  not  to 
introduce  the  disease  with  newly  purchased  fowls  or  to  expose 
healthy  ones  to  the  disease  either  at  or  in  transportation  to 
various  poultry  exhibits. 


GOOSE    SEPTICEMIA  HI 

REFKRENCKS. 


1.  HiGGiNS.  Notes  oil  an  epidemic  of  fowl  cholera  and  upon  the 
comparative  production  of  acid  by  allied  bacteria.  Jour,  of  Experi- 
mental Medicine,  Vol.  Ill  (1898).  p.  651. 

2.  KiTT.  DievSerumimpfunggegenGefliigelcholera.  Monatshefte 
fitr praktische  Tierheilk.,  Vol.  XVI  (1904),  S-  i- 

-.     PERRONCiTO.  Arch.fih-iviss.  u.prackt.  Thierheilk.,  1879,  S.  4- 

4.  Pasteur.  De  I'attenuation  du  virus  du  cholera  des  poules. 
Comptes  rendus  des  Seances  de  V Academic  des  Sciences,  \o\.  XCI 
(1880),  p.  673. 

5.  Pasteur.  Sur  les  maladies  virulentes,  et  en  particulier  sur  la 
maladie  appalee  vulgairement  cholera  des  ponies.  Ibid.  Vol.  XC 
(1880),  p.  239. 

6.  Salmon.  Annual  Reports  of  the  U.  S.  Commissioner  of  Agri- 
culture, 1880-82. 

7.  Salmon.     The  diseases  of  poultry.     Washington,  D.  C.     1889, 

p.  232.  .    ^      . 

8.  Ward.  Fowl  cholera.  Bulletin  No.  136.  College  oj  Agrtc, 
Calif.  Agric.  Exp.  Station,  1904. 


GOOSE  SEPTICEMIA. 

§  93.  Characterization.  The  disease  is  an  acute  sep- 
ticemia causing  the  death  of  the  infected  goose  in  a  few  hours 
after  there  are  evidences  of  sickness. 

§  94  History.  In  1902,  Curtice  described  this  disease 
as  causing  considerable  loss  in  Rhode  Island.  The  following 
note  by  T.  Smith,  dated  October  31,  1900,  quoted  by  Curtice, 
is  significant  in  explaning  the  condition  under  which  the 
disease  disappeared. 

"  Geese  born  in  April  and  May  and  collected  during  the  summer 
and  fall  for  fattening,  kept  in  open  yards,  crowded  together  but  able  to 
move  about ;  about  500  in  a  pen.  Fed  on  a  mixture  of  corn  meal  and 
meat  and  beef  scraps.  Epidemic  began  in  midsummer.  Deaths  up  to 
twenty  a  day  (one  workman  says  sixty  one  day);  about  3,000  lost  to 
date." 

§  95.  Etiology.  The  cause  of  this  disease  is  a  bacterium 
belonging  to  the  septicemia  hemorrhagica  group.      It  is  stated 


112  GOOSE    SEPTICEMIA 

to  have  "  the  characters  of  the  fowl  cholera  type."  It  killed 
rabbits  when  they  were  inoculated  with  0.2  cc.  of  a  bouillon 
culture. 

i^  96.  Symptoms.  The  symptoms  are  indefinite.  In 
the  outbreak  described  the  geese  were  often  found  dead.  The 
description  of  the  disease  by  Curtice  is  appended. 

"  Few  symptoms  of  disease  were  seen,  those  noted  pertain- 
ing mainly  to  the  death  struggles.  Very  few  that  died  were 
noticed  to  be  sick  more  than  an  hour  or  two  before  death, 
and,  as  the  experimental  investigation  demonstrated,  the  dis- 
ease could  not  have  lasted,  in  the  majority  of  the  geese,  more 
than  thirty-six  hours.  An  uncertain  gait,  a  burrowing  of  the 
head  in  the  dirt,  twisting  it  around,  or  actions  indicating 
spasms  of  the  throat,  were  the  earliest  symptoms.  Some 
geese  were  observed  to  die  within  five  minutes  or  after  the 
first  seizure."  There  are  few  chronic  cases  and  recoveries 
are  not  recorded.  Some  show  no  other  symptom  than  being 
slower  in  action,  and  separating  themselves  somewhat  from 
the  flock.  However,  this  sign  is  quite  important  when  the 
wild  nature  and  gregarious  habit  of  the  goose  are  taken  into 
account. 

jj  97.  Morbid  anatomy.  The  tissue  changes,  as  given 
by  Curtice,  are  as  follows  : 

"  There  was  considerable  mucus  in  the  throat  and  mouth, 
and  a  very  tenacious  mucus  in  the  nose.  The  veins  of  the 
head  were  usually  congested,  as  though  the  animal  had  died 
of  asphyxia.  This,  together  with  spasm  of  the  throat,  indi- 
cates a  spasmodic  closure  of  the  glottis.  The  digestive  tract 
was  found  to  be  full  of  food  in  nearly  all  stages  of  digestion. 
In  some  cases  the  catarrhal  products  of  the  intestines  contained 
petechiae.  Sometimes  these  points  were  collected  in  more  or 
less  extensive  patches.  Perhaps  more  than  half  of  the  livers 
showed  yellow  spots  of  from  a  pin  point  to  a  pin  head  in  size. 
These  discolorations  were  found  on  section  to  extend  into  the 
substance  of  the  liver,  and  were  evidently  dead  tissue,  or 
necroses.     In  one  example  the  heart  di.sclosed  severe  inflam- 


DIFFERENTIAL  DIAGNOSIS  I  13 

mation,  botli  epicarditis  and  pericarditis  being  present.  In  one 
case  the  lungs  were  affected.  In  all,  fifteen  cases  were  ex- 
amined, and  from  these  this  composite  description  of  the  post- 
mortem appearances  is  drawn." 

Hemorrhages  on  the  serous  membranes  and  punctate  ne- 
croses in  the  liver  seem  to  be  cjuite  characteristic  lesions. 

Post  })iorlei)i  ;/(?/«.— These  are  a  few  taken  from  Curtice's 
publication. 

"  Goose  No.  I.  Died  last  night ;  quite  fat.  Right  lung,  ventral  por- 
tion quite  firm,  whitish.  Some  flocculi  of  exudate  in  peritoneal  cavity. 
Liver  shows  numerous  point-like  necrotic  foci.  Blood  thick,  blackish 
and  tarry.     Mucus  glassy  on  dusky  mucosae  of  nose  and  throat. 

"  Goose  No.  2.  Died  last  night.  Somewhat  thinner  than  No.  i. 
Ecchymoses  on  fat  in  abdomen  and  gizzard  and  on  heart  muscle  ;, 
necrosis  in  liver.     Blood  thick,  tarry.     Mucus  in  nasal  passages. 

"  Gander  No.  7.  Died  last  night  ;  now  cold.  No  well  marked  hem- 
orrhagic lesion  in  pleuroperitoneal  cavity.  Whitish  points  in  liver. 
Hemorrhagic  or  extremely  hyperemic  condition  of  duodenum.  Jeju- 
num, or  second  coil  of  intestine,  filled  with  a  glairy  mucous  fluid  in 
which  are  suspended  shreds  and  patches  of  food  (?).   Few  if  any  necroses 


§  98.  Differential  diagnosis.  The  disease  here  described 
is  caused  by  Badermm  septicemiae  hemorrhagicae  which  re- 
sembles that  of  fowl  cholera  and  other  members  of  that  group 
of  bacteria.  A  diagnosis,  therefore,  is  made  positive  by  finding 
this  organism  in  the  tissue  of  the  sick  and  dead  geese. 

M'Fadyean  has  described  a  di.sease  undei:  this  title  causing 
the  death  of  many  geese  in  which  he  found  the  blood  swarm- 
ing with  bacteria  suggesting  Bad.  septicemiae  hemorrhagicae 
but  morphologically  different,  but  which  he  could  not  induce 
to  grow  on  any  of  several  media  in  cultures  under  both  aerobic 
and  anaerobic  conditions.  It  appears  that  this  is  a  different 
disease  from  that  described  by  Curtice. 

§  gg.  Prevention.  The  procedure  that  can  be  suggested 
at  present  is  isolation  of  the  well  from  the  sick,  repeating  the 
separations  as  often  as  new  cases  appear.  The  infected  pens 
should  be  thoroughly  disinfected  before  being  reoccupied. 


114  FOWL    TYPHOID 

REFERFNCES. 

1.  Curtice.     Goose  septicemia.   Bulletin  No.  S6,  J\.  I .  Agr.  E\p. 
Station.  1902. 

2.  M'Fadyean.     a    remarkable    outbreak    of    goose  septicemia. 
lour.  Conipar.  Path,  and  Tlierap.,  Vol.  XV  (1902),  p.  162. 


FOWL  TYPHOID. 


§  100.  Characterization.  A  specific  disease  of  fowls 
caused  by  Bacterium  saiiguinarizim.  It  is  not  known  whether 
or  not  other  species  of  domesticated  birds  are  susceptible. 

§  loi.  History.  This  disease  was  briefly  described  by 
Moore  in  1895.  At  that  time  it  had  been  studied  in  but  a  few 
fowls  and  these  the  last  to  die  in  their  respective  flocks.  In 
the  following  year  other  fowls  were  examined  very  carefully 
from  two  outbreaks  of  the  disease  and  it  is  upon  the  data 
obtained  in  their  investigation  together  with  those  procured 
from  many  produced  cases  that  the  description  of  the  disease 
is  based.  It  was  described  as  an  infectious  leukemia.  Further 
investigation,  however,  has  shown  that  the  excess  of  white 
corpuscles  was  due  to  a  leucocytosis  brought  about  by  the  in- 
fecting organism  and  that  the  disease  is  not  a  true  leukemia. 

It  was  found  by  Smith  in  1894,  on  Block  Island,  R.  I. 
In  1898,  Dawson  found  it  to  be  the  cause  of  very  serious  losses 
among  poultry  near  Baltimore,  Md.  In  all  of  the  outbreaks 
studied,  the  owners  of  the  fowls  first  reported  the  disease  as 
-chicken  cholera.  In  1902,  Curtice  investigated  an  outbreak  in 
Rhode  Island. 

§  102.  Geographical  distribution.  It  was  first  studied 
in  fowls  taken  from  an  outbreak  in  Virginia.  Since  then,  it 
has  been  identified  in  Maryland,  the  District  of  Columbia,  and 
the  State  of  Rhode  Island.  There  is  good  evidence  in  the 
numerous  reports  of  destructive  fowl  diseases  to  believe  that  it 
is  quite  widespread  in  the  United  States.  Thus  far,  there 
seems  to  be  no  reports  of  its  extent  in  other  countries. 


ETIOLOGY  115 

ji   103.     Etiology.     Moore  isolated  and  described  a  patho- 
genic bacterium  which  he  designated  Bacterium  sanguinarhim . 
With  this  organism  the  disease  has  been  produced   in  healthy 
fowls  both  by  feeding  cultures  and  l)y 
intravenous  injections.      Its  etiological  ^ -, 

relation  to   the   disease    is,  therefore,  r-  •j^/3 

quite  clearly  established.     It  is  possi-  -        l^^^*^ 

ble  that  certain  accompanying  condi-  '^  . 

tions  may  be  necessary  in  conjunction         ^  V 

with  the  organism  to  cause  the  dis- 
ease   to    spread    rapidly    in    a     flock. 

Experimentally  it  did  not  spread  from  ^^^  ^^  ^  ^^^^^  ^^^^^. 
diseased  (inoculated  or  fed)  to  healthy  terhmi  safiguinarium  hi 
fowls  when  kept  in  the  same  yard.  a  blood  space  in  the  liver 

{much  enlarged). 
^  104.  Symptoms.  From  the 
statement  of  the  owners  of  the  diseased  fowls  in  the  different 
outbreaks  and  from  the  appearance  of  those  in  which  the  dis- 
ease was  artificially  produced,  little  can  be  positively  stated 
concerning  the  early  symptoms.  There  is  a  pronounced  anemic 
condition  of  the  mucosa  of  the  head.  An  examination  of  the 
blood  shows  a  marked  diminution  in  the  number  of  red  corpus- 
cles and  an  increase  in  the  number  of  white  ones.  In  the  dis- 
ease produced  artificially  by  feeding  cultures  of  the  specific 
organism  there  are,  in  most  cases,  a  marked  drowsiness  and 
general  debility  manifested  from  one  to  four  days  before  death 
occurs.  The  period  during  which  the  prostration  continues 
varies  from  a  few  hours  to  two  days.  The  mucous  membranes 
and  skin  about  the  head  become  pale.  There  is  an  elevation  of 
from  I  to  4  degrees  in  temperature.  The  fever  is  of  a  contin- 
uous type,  as  shown  in  the  appended  temperature  chart  of  two 
fowls  in  which  the  disease  was  produced  artificially. 

Although  the  course  of  the  disease  in  different  fowls  is 
usually  constant,  there  are  many  variations.  The  time 
required  for  fatal  results  is  from  three  to  fifteen  days,  but  ordi- 
narily death  occurs  in  about  eight  days  after  feeding  the  cul- 
tures.    The  rise  in  temperature  can  be  detected  about  the  third 


i6 


FOWL    TYPHOID 


day  and  external  symptoms  about  the  fifth  or  sixth,  occa- 
sionally not  until  a  few  hours  before  death.  The  symptoms 
observed  in  the  cases  produced  by  feeding  correspond  with 
those  described  by  the  owners  of  affected  flocks. 

As  indicated  in  the  inoculation  experiments,   the  symp- 
toms following  the  intravenous  injection  of  the  virus  were,    as 


^ 

^^ 

^ 

1      ,D. 

ad. 

/r- 

'"-'' 

^-^ 

o^ 

^^- 

--' 

f/O. 

V'' 

^ 

-^ 

/ 

r 

r^ 

-  ^. 

^ 

-■'/ 

■^  \ 

\ 

/ 

^ 

■^^ 

,  y 

^^ 

f— 

, 

f>~- 

■-:.-_l- 

'/ 

Fkv.  i6.      Temperature  chart  of  trvo  fatal  cases  artificially 
produced  in  foTcls. 


would  be  expected,  considerably  modified  from  those  fowls 
which  contracted  the  disease  by  the  ingestion  of  cultures  of  the 
specific  bacterium. 

i^  105.  Morbid  anatomy.  The  only  constant  lesions 
found  in  the  fowls  which  contract  the  disease  naturally,  as 
well  as  in  those  fed  upon  the  virus,  are  in  the  liver  and  blood. 
The  liver  is  somewhat  enlarged  and  dark  colored.  A  close 
inspection  shows  the  surface  to  be  sprinkled  with  minute 
grayish  areas.  The  microscopic  examination  shows  the  blood 
spaces  to  be  distended.  The  hepatic  cells  often  stain  very 
feebly.  Not  infrequently  the  cells  are  isolated  and  their  out- 
lines indistinct.  Occasionally  foci  are  observed  in  which  the 
liver  cells  appear  to  be  dead  and  the  intervening  spaces  infil- 
trated with  round  cells.  The  changes  in  the  hepatic  tissues 
are  presumably  secondary  to  the  engorgement  of  the  organ 
with  blood. 

The  rareness  with  which  the  intestinal  tract  is  affected  in 
both  the  natural  and  artificially  produced  cases  is  exceedingly 


MORBID    ANATOMY  "7 

interesting  and  important  for  the  differential  diagnosis.  There 
is  in  most  cases  a  hyperemia  of  the  mucous  membrane  of  the 
colon,  but  this  condition  is  not  uncommon  in  the  healthy  indi- 
vidual. The  kidneys  are  generally  but  not  uniformly  pale. 
Thev  are  streaked  with  reddish  lines,  due  to  the  injection  of 
blood  vessels.  In  section  the  tubular  epithelium  appears  to  be 
normal.  The  kidneys  seem  to  be,  from  the  number  of  bacteria 
in  the  cover-glass  preparations,  especially  favorable  for  the 
localization  of  the  specific  organism.  The  spleen  is  rarely  dis- 
colored or  engorged  with  blood.  The  lymphatic  glands  were 
not  appreciably  enlarged  in  any  individual  examined.  The 
lungs  except  in  chronic  cases  are  normal.  The  brain  and 
spinal  cord  are  unaffected. 

The  heart  muscle  is  usually  pale  and  sprinkled  with  gray- 
ish points,  due  to  cell  infiltration  and  necrosis.  These  lesions 
are  so  common  that  it  seems  safe  to  consider  them  character- 
istic manifestations.  Death  usually  occurs  in  systole,  the 
auricles  containing  very  thin,  unclotted  blood. 

The  most  important  alterations  are  found  in  the  blood. 
These  consist,  in  the  progress  of  the  disease,  of  the  gradual 
disappearance  of  the  red  corpuscles  and  increase  in  the  number 
of  white  ones,  as  determined  by  blood  counts  made  daily  or 
every  other  day,  from  the  time  of  inoculation,  or  of  feeding 
the  virus,  until  the  day  of  death. 

The  diminution  in  the  number  of  red  corpuscles  and  the 
increase  in  the  number  of  white  ones  are  illustrated  in  the 
blood  count  of  two  cases  of  artificially  produced  disease. 

In  carefully  heated  cover-glass  preparations  of  healthy 
fowl's  blood  stained  with  methylene-blue  and  eosin,  the  nuclei 
are  colored  a  deep  blue,  and  the  cellular  protoplasm  surround- 
ing the  nucleus  is  stained  by  the  eosin.  In  similar  prepara- 
tions made  from  the  blood  of  the  affected  fowls  there  are  a 
greater  or  less  number  of  cells  which  do  not  take  the  eosm 
stain.  These  were  called  spindle  cells  by  Van  Reckling- 
hausen, blood  plates  by  Bizzozero,  and  hematoblasts  by 
Hayem.  More  recently  Dekhuyzen  has  called  them  throm- 
bocytes.    In  these  the  portion  of  the   cell    body    surrounding 


i8 


FOWL    TYPHOID 


the  nucleus  remains  unstained  or  becomes  slightly  tinted  with 
blue.  Occasionally  they  contain  one  or  more  vacuoles,  and 
the  margin   is   frequently    broken.     The   apparent   dissolving 

away  of  the  red  corpuscles 
has  been  frequently  ob- 
served  and  corpuscles 
showing  the  intermediate 
stages  are  readily  detected 
in  carefully  prepared  speci- 
mens. These  must  be  dif- 
ferentiated from  the  blood 
plates. 

The  cause  of  the  de- 
struction of  the  red  cor- 
puscles is  not  satisfactorily 
explained.  In  his  report 
on  fowl  cholera,  Salmon  il- 
lustrates leucocytes  sur- 
rounding the  red  corpus- 
cles, but  the  marked  di- 
minution of  the  red  cells 
was  not  determined.  He 
speaks,  however,  of  the 
pale  color  of  the  blood.  In  fresh  preparations  of  the  blood, 
portions  of  red  cells  may  be  seen  within  the  leucocytes,  those 
containing  spindle  shaped  granules.  The  determination  of 
the  extent  of  this  mode  of  destruction  of  the  red  corpuscles 
necessitates  further  investigation. 

tabi^e;  showing  changes  in  the  number  of  corpusci^es. 

Fowl  No.  82,  inoculated  in  the  wing  vein,  February  6. 


Fig.  17.  Blood  from  a  iv  ell  advanced 
case  of  fowl  typhoid  showing  red 
corpuscles^  blood  plates  and  increase 
in  the  number  of  leucocytes. 


Number  of 

Number  of 

Date 

Tempera- 
ture (F°.) 

red  cor- 
puscles, 
per  c.  mm. 

white  cor- 
puscles 
per  c.  mm. 

Remarks 

Feb.  6 

107.4 

3.744.444 

21,222 

Well. 

7  :       109 

3.417,391 

26,087 

Apparently'  well. 

8  1         108.2 

2,784.700 

55,000 

Do. 

9  I         108.4 

2,807,692 

76,925 

Do. 

11  1         107.4 

3.481,818 

90,909 

Feathers  ruffled  ;  refuses  food. 

13  1         110.2 

2,133,333 

100  000 

Very  quiet  ;  comb  pale. 

14  1         108 

2,530,000 

140,000 

Fowl  died  later  in  the  day. 

MORBID    ANATOMY 


119 


Fowl  No.  501,  fed  culture  March  26. 


Mar.  26 

28 

Apr.   2 

3 


Xumber  of!  Number  of 
red  cor-  white  cor- 
puscles    I     puscles 

per  c.  mm.  per  c.  mm. 


166.2 


3,53500° 
no  2,430,000 

110.6  I  684,210 

106  I     1,745.000 


1^,940 
70.000 
80,000 
245.000 


Well. 

Fowl  eats  very  little. 
Blood  verv  pale:  fowl  weak;  refuses  food. 
Verv   weak;  many    red    corpuscles    at- 
tacked by  leucocytes. 
Found  dead. 


In  fresh  preparations  of  the  blood  of  affected  fowls  exam- 
ined in  Toisson's  fluid,  red  corpu.scles  which  take  the  violet 
stain  more  or  less  intensely 
throughout  are  frequently 
observed. 

In  the  blood  of  poultry 
two  distinct  classes  of  white 
corpuscles  are  conspicuous. 
The  first  which  predomin- 
ates in    numbers,   contains 
nuclei   with    from    one    to 
four  lobes,    and    the    cyto- 
plasm is  sprinkled  with   a 
variable  number  of  round, 
elongated,  or  spider- shaped 
bodies.     In  the  fresh  con- 
dition  they  are  highly  re- 
fractory.    They  stain  with 
eosin,  and  if    the  prepara- 
tions are  heated  sufficiently 
thev  will   retain   certain   of 
the'  aniline  dyes.     The  other  class  consists  of  round  or  nearly 
round  cells  which  takes  the  blue  stain  feebly.     Usually  it  is 
difficult  to  detect  the  nucleus,  although  it  is  occasionally  dis- 
tinct      Between  these    two  types   there  are   many   varieties. 
The  leucocytes  containing  the  spindle-shaped  bodies  appear  to 
be  the  phagocytes,    as  they  were  the  only  ones  which  were 
observed  to  engulf  the  red  corpuscles.     Bacteria  have  not  been 
demonstrated  in  these  cells,  although  their  presence   has,  in 


.s7/o: 


Section    of   chicken's    liver 
'inq;  blood  engorgement. 


FOWL    TYPHOID 


several  cases,  been  suspected.  From  the  appearances  observed 
in  the  red  blood  corpuscles  it  seems  highly  probable  that 
phagocytosis  plays  a  comparatively  large  part  in  their  destruc- 
tion. Another  hypothesis  is  also  suggested,  namely,  that  a 
toxin  produced  during  the  multiplication  of  the  specific  organ- 
ism has  this  effect 
on  the  red  corpus- 
cles. In  the  fresh 
preparations  w  e 
can  observe  the 
phagocytes  attack- 
ing the  red  cells. 
In  the  stained  ones 
mutilated  red  cor- 
puscles and  free 
nuclei  are  present. 
The  hypothesis  is 
suggested  that  the 
leucocytes  partially 
digest  certain  of 
the  red  corpuscles 
in  their  attack  up- 
on them.  Whether 
to    the    phagocytes 


Fig.  19.  The  phagocytic  action  of  the  white 
blood  corpuscles  upon  the  red  ones  in  advanced 
cases.  The  changes  represented  fron  i  to  g 
took  place  in  jj  minutes. 

ittributable 


these   changes    are    entirely 
is  an  open  question. 

In  the  blood  from  healthy  fowls  it  is  comparatively  rare 
to  see  one  of  the  white  corpuscles  engulfing  a  red  one.  As  the 
disease  progresses,  however,  this  warfare  becomes  very  con- 
spicuous, owing  perhaps  to  the  increased  number  of  the  color- 
less cells.  Up  to  the  present  the  study  of  these  corpuscles  has 
not  been  extended  beyond  the  observations  of  the  general  ap 
pearance  of  these  structures,  and  no  attempt  is  made  to  explain 
the  apparently  marvelous  increase  in  the  number  of  the  leuco- 
cytes. It  is  an  interesting  and  as  yet  unexplained  fact  that 
the  increase  in  the  corpuscles  is  apparently  restricted  to  those 
containing  the  spindle  shaped  bodies. 

§   106.     Differential  diagnosis.     Intestinal  disturbances, 


DIFFKRENTIAI.    DIAGNOSIS 


especially  diarrhea  and  fowl  cholera,  are  the  diseases  liable  to 
be  mistaken  for  fowl  typhoid. 

A  comparison  of  the  important  changes  in  the  morbid 
anatomy  in  fowl  cholera,  as  described  by  European  writers, 
and  in  the  disease  under  consideration,  can  be  made  from  the 
appended  columns,  in  which  their  more  characteristic  lesions 
are  contrasted  : 


Lesions  in  fowl  cholera. 

Duration  of  the  disease  from  a 
few  hours  to  several  days. 

Elevation  of  temperature. 

Diarrhea. 

Intestines  deeply  reddened. 

Intestinal  contents  liquid,  mu- 
copurulent, or  blood  stained. 

Heart  dotted  with  ecchymoses. 


7.  Lungs  affected,  hyperemic  or 

pneumonic. 

8.  Specific  organisms  appear    in 

large  numbers  in  the   blood 
and  organs. 

9.  Blood  pale   (cause   not    deter- 

mined). 

10.  Condition  of  leucocytes   not 

determined. 


Lesions  in  foivl  typhoid. 

1.  Duration  of  the  disease  from  a 

few  hours  to  several  days. 

2.  Elevation  of  temperature. 

3.  Diarrhea  not  common. 

4.  Intestines  pale. 

5.  Intestinal  contents   normal  in 

consistency. 

6.  Heart  usually  pale  and  dotted 

with  grayish  points,  due  to 
cell  infiltration. 

7.  Lungs   normal,    excepting    in 

modified  cases. 

8.  Specific    organisms    compara- 

tively few  in  the  blood  and 
organs. 

9.  Blood   pale,    marked    diminu- 

tion in   the  number  of   red 
corpuscles. 

10.  Increase    in    the    number    of 

leucocvtes. 


Attention  should  be  called  to  the  fact  that  as  yet  there 
seems  not  to  have  been  a  careful  study  of  the  condition  of  the 
blood  in  fowl  cholera.  Salmon  observed  many  changes  which 
may  have  been  similar  to  or  identical  with  those  herein 
recorded.  Ward  found  an  increase  in  the  number  of  white 
corpuscles  and  in  some  cases  a  decrease  in  the  number  of  red 
ones  in  cases  of  fowl  cholera. 

The  difference  between  the  specific  organism  of  these  two 
diseases  can  be  readily   appreciated    by    a    comparison    of  the 


FOWL     TYPHOID 


more   diagnostic    properties   of  each 
parallel  columns,  as  follows  : 


they    are    arranged 


BacteriiDit  of  foivl  cholera. 

Bacterium    short,     with      oval 
ends. 


It   usually 
tissues. 


appears  singly    in       2. 


Ordinarily  it  exhibits  a  polar 
stain  (from  tissue). 


( Trows  feebly  or  not  at  all  on 
gelatin. 

It  does  not  change  milk. 

Resists  drying  from  one  to 
three  days. 

Kills  rabbits  inoculated  sub- 
cutaneously  in  from  eigh- 
teen  to  twentv-four    hours. 


It  kills  fowls  when  injected 
subcutaneously  in  small 
quantities. 


Bacterium    sangu  inariu  ni . 

Bacterium  short,  with  ends 
oval  or  more  pointed. 

It  usually  appears  in  pairs 
united  end  to  end  or  in 
clumps  in  tissues. 

It  gives  a  light  center,  with 
uniformly  stained  periphery 
(from  tissue).  Rarely  a 
polar  stain  is  observable. 

Decided  growth  on  alkaline 
gelatin. 

Saponifies  milk. 

Resists  drying  from  eight  to 
twelve  days. 

Kills  rabbits  inoculated  intra- 
venously in  from  three  to 
five  days.  Rabbits  inocu- 
lated subcutaneously  remain 
well  or  die  in  from  six  to 
ten  days. 

It  does  not  kill  fowls  when  in- 
jected subcutaneous]}-  in 
small  quantities. 


While  there  are  many  similarities  in  the  symptomatology 
of  these  two  diseases,  there  are  pronounced  differences  in  the 
morbid  anatomy  and  in  the  specific  microorganisms.  These 
facts  render  positive  differentiation  dependent  upon  a  care- 
ful bacteriological  and  pathological  examination.  In  fowl 
cholera  the  course  of  the  disease  is  more  rapid  than  in  fowl 
typhoid. 

§  107.  Prevention.  Prompt  isolation  of  the  well  from 
the  sick  fowls  and  thorough  disinfection  of  the  houses  and 
yards. 

In  reference  to  preventing  its  introduction,  Curtice  makes 
the  following  observation  ; 


SWINE    ERYSIPELAS  I  23 

"  Inasmuch  as  one  possible  method  of  introducing  the 
disease  is  through  purchases,  it  will  always  be  necessary  for 
purchasers  to  enquire  into  the  history  of  the  flock  from  which 
additions  are  to  be  made,  and  especially  to  examine  into  the 
condition  of  the  fowls.  It  is  better  in  any  case  to  keep  new 
purchases  by  themselves  for  some  weeks  or  until  it  is  apparent 
that  they  are  healthy." 

REFERENCES. 

1.  Curtice.  Fowl  typhoid.  Bulletin  Sj.  Agr.  Exp.  Station  of 
the  R.  I.  College  of  Agric.  and  Mech.  Arts,  1902. 

2.  Dawson.  Infectious  leukemia.  Annual  Report  of  the  Bureau 
of  Animal  Industry,  U.  S.  Dept.  Agric.,  1898. 

3  MooRE.  A  study  of  a  bacillus  obtained  from  three  outbreaks  of 
fowl  cholera.    Bulletin  No.  S,  U.  S.  Bureau  of  Animal  htdustry,  1895. 

4  Moore  Infectious  leukemia  in  fowls-A  bacterial  disease 
frequently  mistaken  for  fowl  cholera.  Annual  Report  of  the  Bureau 
of  Animal  Industry,  1895-96. 


SWINE  ERYSIPELAS. 
Synonyms.  Red  fever  of  swine  ;  rougcf  ;  Rotlatij. 
%  108.  Characterization.  This  disease,  peculiar  to 
swine,  is  determined  by  a  rise  of  temperature,  cerebral  distur- 
bances and  pronounced  reddening  of  areas  of  the  skin.  It  is 
a  disease  of  adult  life.  It  is  stated  that  pigs  are  rarely  attacked 
under  three  months  or  over  three  years  of  age.  Lydtm  and 
Schottelius  found  some  differences  in  the  degree  of  suscepti- 
bility of  certain  breeds  of  swine.  The  common  country  pig 
was  least  susceptible. 

§  109.  History.  This  disease  has  been  known  in 
Europe  for  many  years.  Smith  found  a  bacterium  in  rabbits 
inoculated  with  the  organs  of  pigs  that  had  died  of  an  unde- 
termined disease  in  Minnesota,  which  was  either  the  bacterium 
of  swine  erysipelas  or  of  mouse  septicemia.  The  latter  organ- 
ism had  been  recorded  on  two  previous  occasions  from  pigs  in 
this  country. 


124  SWINE    ERYSIPELAS 

§  1 10.  Geographical  Distribution.  Swine  erysipelas 
is  an  infectious  disease  that  occurs  enzootically  and  in  epi- 
zootics in  most  of  the  countries  of  Europe.  It  was  formerly 
restricted  in  Bavaria  to  the  districts  along  the  Danube,  and 
was  entirely  unknown  in  southern  Bavaria  (Kitt).  It  is 
stated  that  the  disease  tends  to  become  enzootic  chiefly  in 
valleys  and  low-lying  plains  which  have  slow-flowing  streams 
and  heavy,  damp,  claj^  soil  ;  and  that  sandy  and  granite  soils 
are  comparatively  free  from  it.  It  occurs  chiefly  during  the 
months  of  July,  August  and  September,  although  it  appears 
sporadically  during  the  winter  m.onths.  It  has  not  been 
described  from  the  United  States. 

§111.     Etiology.    Loeffler  and  Schiitz 
'(^  ^'^^^/"^-^  pointed  out  in   1885  that  swine  erysipelas 

•V     ^^•'^^f'^  /        was  caused   bv    a    very    slender   bacterium 
-'■""  {Bad.   erysipelatis  suis)    i   to  2//  long    and 

0.3  to  0.4//  broad,  straight  or  slightly 
curved,  ends  not  rounded  and  in  cultures 
Fig.  20.  Bacter-  often  appearing  in  filaments.  It  is  very 
ium  of  swine  ery-  closely  related  to  the  bacterium  of  mouse 
sipelas,  showing  septicemia  described  bv  Koch  in  1878.  In 
free    organisms      ^  .^^ere    the    bacterium    of    mouse 

a  nd  al  so    tn^j  r  '^       .      . 

presence   'a' it h  in      septicemia  is  quite  common,  swine  erysipe- 
the  cells.  las    prevails.      There  is  much  uncertainty 

concerning  the  relationship  of  the  bacter- 
ium of  mouse  septicemia  to  that  of  this  disease.  Smith  has 
suggested  that  possibly  the  bacterium  which  has  been  found 
in  this  country  may  gain  virulence  sufficient  to  produce  epi- 
zootics, if  such  is  not  already  the  case.  It  is  exceedingly 
important  that  careful  search  be  made  for  this  organism  in  the 
outbreaks  among  swine  where  the  nature  of  the  disease  is  not 
clearly  determined.  House  mice  and  pigeons  are  susceptible 
to  the  bacteria  of  swine  erysipelas  ;  guinea  pigs  and  fowls  are 
immune.  Rabbits  suffer  from  erysipelatous  swellings  when 
inoculated  subcutaneously  in  the  ear.  The  bacterium  of 
swine  erysipelas  is  to  be  differentiated  from  that  of  mouse 
septicemia. 


SYMPTOMS  ^25 

The  period  of  incubation  is  stated  to  be  at  least  three  days. 
It  is  apparently  longer  than  that  in  many  cases. 

^   112.     Symptoms.     The  disease   usually    begins    sud- 
denly and  violently.      The  animal  refuses  food,    makes  efforts 
to  vomit,  has  a  rise  of  temperature,   manifests  severe  nervous 
disturbance,  is  very  weak,  torpid    and    indifferent    to   its    sur- 
roundings.    When  approached  it  tries  to  hide  itself  under  its 
bedding.      The  hind   quarters  become  weak  and    paralyzed. 
Muscul^ar  spasms  and  grinding   of    the    teeth    are   sometimes 
observed.     At  first  there  is  constipation,  the  conjunctiva  is  of 
a  dark  red  or  brownish-red  color,  and  the  eyelids  are  some- 
times swollen.     Usually  a  day  or  two  after  the  first  symptoms 
develop  or,  perhaps,  from  the  first,    reddish   spots  appear   on 
the  thin  parts  of  the  skin,  such    as  the    region   of  the   navel, 
lower  surface  of    the  chest,    perineum,    inner   surface   of  the 
thighs,  ears  and  throat.     These  spots,  which  at  first  are  bright 
red  and  about  the  size  of  a  man's  hand,  become,  later  on,  dark 
red  or  purple,  and  soon    unite   into   large,    irregularly-shaped 
patches.     As  a  rule,  they  are  neither  painful  to  the  touch  nor 
prominent,  but  sometimes   they   show   a  slight   inflammatory 
swelling.     The  skin  of  the  red  spots,  especially  of  the  ears, 
may  suffer  from  an  eruption  of  vesicles  and  may   even  slough. 
The  reddening  of  the  skin  may  be  very  slight  in   severe  cases, 
or  mav  appear  only  immediately  before,    or  even   after,  death. 
Death  takes  place  usually  on  the  third  or  fourth  day.     In  the 
very  severe  form,  the  animal  may  die  in   twenty-four  hours, 
otherwise  the  disease  requires   a    week    or   longer    to    run    its 
course. 

Jensen  considers  that  this  disease,  instead  of  being  uniform 
in  its  clinical  aspects,  manifests  itself  in  the  following  forms, 
which  differ  from  each  other  by  well-marked  peculiarities. 
The  forms  recognized  as  varieties  of  this  disease  but  more 
generally  considered  as  distinct  maladies  and  known  by  differ- 
ent names  are  as  follows  : 


1.  True  erysipelas. 

2.  Swine  urticaria. 


126  SWINE    ERYSIPELAS 

3.  Erysipelas  without  redness  of  the  skin. 

4.  Diffuse  necrotic  erysipelas  of  the  skin. 

5.  Endocarditis  of  erysipelas. 

He  also  maintains  that  there  may  sometimes  be  transi- 
tional forms  between  the  respective  varieties  which  he  enumer- 
ates. Different  forms  of  epizootic  erysipelas  have  also  been 
described  by  Cornevin,  Hess  and  others. 

§  113.  Morbid  anatomy.  In  the  ordinary  form  of  epi- 
zootic erysipelas  there  is  a  septicemic  condition  without  any 
well  marked  morbid  changes  of  separate  organs.  In  less  acute 
cases  the  septicemia  may  give  way  to  hemorrhagic  and  diph- 
theritic gastro-enteritis,  considerable  swelling  of  the  lymphatic 
system,  hemorrhagic  or  parenchymatous  nephritis,  and 
hepatitis,  acute  swelling  of  the  spleen  and  myositis.  The 
hemorrhagic  gastro-enteritis  consists  at  first  of  excessive 
inflammation  of  the  mucous  membrane  of  the  stomach  in  the 
region  of  the  fundus.  The  mucosa  shows  a  dark-red  discolor- 
ation which  is  partly  diffuse  and  partly  in  spots.  The  cells 
suffer  from  cloudy  swelling  and  the  mucous  membrane  is 
covered  with  a  viscid  layer  of  mucus.  The  intestinal  mucous 
membrane  is  swollen,  especially  on  the  top  of  the  folds  and  in 
the  neighborhood  of  Peyer's  patches.  It  is  infiltrated  with 
blood  and  sometimes  shows  superficial  scabs.  Less  frequently, 
circumscribed  parts  of  the  mucosa  of  the  cecum  and  the  anter- 
ior parts  of  the  colon  suffer  from  a  diphtheritic  affection. 

The  solitary  follicles  and  Peyer's  patches  appear  as  prom- 
inently raised  patches.  Sometimes  they  are  infiltrated  with 
blood  and  surrounded  by  a  reddish  band.  There  is  ulceration 
and  cicatrization  of  the  solitary  and  agminated  follicles.  The 
mesenteric  glands  become  more  swollen  than  the  other  glands 
of  the  body,  of  a  dark  red  color,  and  show  softening.  The 
surface  of  fresh  sections  is  dun-colored  with  interspersed  dark- 
red  areas.  The  paraglandular  tissue  is  hyperemic  and  infil- 
trated with  blood. 

The  kidneys  are  enlarged,  the  cortex  of  a  grayish-red  and 


DIFFERENTIAL    DIAGNOSIS  I  27 

the  medullary  portion  of  a  very   dark-red  color.      Frequently 
catarrhal  nephritis  occurs  as  a  complication. 

The  acute  swelling  of  the  spleen  arises  in  consequence  of 
an  acute  hyperemia,  with  an  increase  of  the  cellular  constitu- 
ents of  the  pulp,  in  which  case  the  organ  is  enlarged,  but  not 
softened  as  in  anthrax.  The  pulp  is  of  a  purple  color,  moder- 
ately soft  and  free  from  hemorrhages. 

There  is  cloudy  swelling  and  enlargement  of  the  liver. 
The  surface  of  sections  has  a  grayish-brown  color,  and  the 
acini  are  widened.  The  muscles  are  gray  in  color,  soft,  flac- 
cid, watery,  glistening  and  sometimes  they  are  sprinkled  with 
hemorrhages.  They  give  the  general  appearance  of  boiled 
flesh.  The  myocardium  shows  similar  spotted  changes,  and 
punctiform  hemorrhages  beneath  the  endocardium.  In  the 
abdominal  and  thoracic  cavities  and  pericardium,  there  may 
be  found  small  quantities  of  an  orange-colored,  clear  fluid, 
which  may  be  mixed  with  a  flaky  coagulum. 

Many  English  veterinarians  regard  the  occurrence  of 
more  or  less  luxuriant  vegetations  on  the  valves  of  the  heart 
to  be  so  common  that  it  is  to  be  considered  almost  diagnostic. 
It  would  appear  from  the  literature  that  this  endocarditis  is 
not  nearly  so  common  in  continental  Europe.  The  lungs 
remain  unchanged,  or  at  most  exhibit  a  post-mortem  edema. 
By  microscopic  examination,  the  specific  bacteria  are  found 
everywhere  in  the  body,  especially  in  the  spleen  and  kidneys, 
and  to  a  less  extent  in  the  blood. 

The  duratio7i  of  the  disease  varies  from  i  to  10  days.  In 
types  of  moderate  severity  it  runs  from  3  to  4  weeks. 

The  prognosis  is  unfavorable.  There  is  from  20  to  80  per 
cent  mortalit3\ 

§  114.  Differential  diagnosis.  Swine  erysipelas  is  to 
be  differentiated  from  : 

I.  Hog  cholera  and  swine  plague.  The  frequent  red- 
dening of  the  skin  in  these  diseases  together  with  the  modified 
lesions    so    frequently    observed    may    cause    confusion.     The 


128  SWINE    ERYSIPELAS 

bacteriological  examination  will  enable  the  positive  diagnosis 
to  be  made.      (See  hog  cholera  and  swine  plague.) 

2.  Anthrax,  which  is  very  rare  in  swine.  Here,  too, 
the  bacteriological  examination  discloses  the  true  nature  of  the 
disease. 

3.  Er3'themata  due  to  various  dietary  causes. 

The  significance  of  a  deep  reddening  of  the  skin  about  the 
head,  abdomen  and  thighs  of  pigs  is  not  fully  determined. 
It  is  clear,  however,  that  such  a  condition  often  occurs  in  the 
absence,  so  far  as  present  knowledge  goes,  of  a  specific  infec- 
tion. It  is  frequently  found  in  pigs  suffering  from  digestive 
troubles,  or  poisoning  from  eating  decomposed  offal. 

§  115.  Preventive  inoculation.  Pasteur's  preventive 
inoculation  was  until  recently  the  chief  prophylactic  means 
employed  against  epizootic  erysipelas.  Metchnikoff  found 
that  the  blood  of  immunized  rabbits  was  antitoxic,  and  L,orenz 
maintains  that  the  serum  of  swine  that  have  recovered  from 
swine  erysipelas  is  also  antitoxic,  and  will  produce  immunity 
in  other  animals.  The  treatment  introduced  by  Lorenz  is  to 
inject  the  immunizing  serum  in  the  proportion  of  i  cc.  to  every 
10  kilograms  of  the  body  weight  of  the  animal.  Two  days 
afterward  o. 5  to  i.o  cc.  of  virulent  culture  is  injected,  and 
after  twelve  days  the  dose  is  doubled.  The  use  of  the 
immunizing  serum  is  reported  to  be  very  successful. 

REFEREN'CKS. 

1.  Bang.  Ueber  Rotlauf-Eudocarditis  bei  Schweinen.  Deutsche 
Zeitschr.f.  Thietmed.,  Bd.  XVIII  (1891),  S.  27. 

2.  Jensen.  Die  Aetiologie  des  Nesselfiebers  und  der  diffusen 
Hautnekrose  des  Schweines.  Deutsche  Zeitschr.  f.  Thierined.,  1892, 
S.  278. 

3.  LOEFFLER.  Experimentelle  Untersuchutigen  iiber  Schweine- 
Rotlauf.  Arbeiten  aus  d.  Kaiserlichen  Gesundheitsamte,  Bd.  i  (1885), 
S.  46. 

4.  LoRENZ.  Die  Schutzimpfung  gegeii  Schweinerotlaiif  mit 
Anwendung  eines  aus  Blutserum  immunisirter  Thiere  hergestellten 
Impfstoffes.     Deutsche  Zeitschr./.  Thierrned.,  Bd.  XX  (1894),  S.  i. 


ANTHRAX  129 

5.  LoRENZ.  Die  Veterinarpolizeiliche  Behandhmg  des  vSchwein- 
erothlaufes  und  die  Schutzimpfung.     Berliner  thierarz.  Wochen.,  1897, 

s.  574. 

6.  LoRENZ.  Schut/.impfungeii  gegen  den  Rotlauf  der  Schweine. 
Ibid,  1897,  S.  109. 

7.  Moore.  Mouse  septicemia  bacilli  in  a  pig's  spleen  with  some 
observations  on  their  pathogenic  properties.  Jour,  of  Comp.  Med.  and 
Vet.  Archives,  Vol.  XIII  (1892),  p.  333. 

8.  Pasteur  ET  Thuillier.  La  vaccination  du  rouget  des  pores  a 
Paide  du  virus  mortel  attenue  de  cette  maladie.  Comp.  rend  us  Acad, 
des  Sciences,  Vol.  XCVII  (1883),  p.  1163. 

9.  SCHUTZ.  Ueber  den  Rotlauf  der  Schweine  und  die  Impfung 
mil  demselben.  Arbeit  a.  d.  Kaiserlichiu  Ccsundlieistanitc,  Bd.  I 
(1885),  S.  56. 

10.  vSmith.  An  Kxamination  of  Pasteur's  Vaccine  for  Rouget. 
Annual  Report  U.  S   Bureau  of  Animal  Industry,  1885,  p.  187. 

ir.  Smith.  Swine  erysipelas  or  mouse  septicemia  bacilli  from  an 
outbreak  of  swine  disease.  A?inual  Rept.  U.  S.  Bureau  of  Animal 
Industry,  1895-96,  p.  166. 


ANTHRAX. 


Synonyms.  Splenic  fever  ;  splenic  apoplexy  ;  wool 
sorters'  disease  ;  malignant  pustule  ;  anthracemia  ;  mycosis 
iutestinalis  ;  charbon  ;  Milzbrand. 

§  116.  Characterization.  Anthrax  is  an  infectious 
disease  occurring  sporadically  and  in  epizootics  in  herbivora 
and  omnivora  and  communicable  to  nearly  all  warm-blooded 
animals,  and  to  man.  It  is  characterized  by  the  presence  in 
the  diseased  tissues  or  liquids  of  Bacterium  anthracis,  by  an 
enlarged  spleen,  blood  extravasations  and  by  local  gangrene. 
It  usually  occurs  in  the  acute  form. 

§  117.  History.  Anthrax  is  among  the  oldest  of  the 
known  infectious  diseases  of  animals.  Descriptions  of  epi- 
demics and  epizootics  of  this  disease  are  given  by  Homer, 
Plutarch,  Livy  and  other  writers  before  the  Christian  Era. 
The  Arab  physicians  designated  it  as  "Persian  Fire."  Exten- 
sive outbreaks  are  mentioned  in  the  literature  of  the  fifteenth, 
sixteenth,  seventeenth,    eighteenth   and   nineteenth   centuries. 


T30 


ANTHRAX 


Chabert  pointed  out  in  1780  that  the  various  kinds  or  forms 
of  the  disease,  which  had  previously  been  described  as  independ- 
ent affections,  were  all  one  disease.  As  late  as  1805,  Kausch 
gave  a  good  description  of  anthrax  but  denied  its  contagious- 
ness. Delafond  and  Gerlach  thoroughly  investigated  ovine 
anthrax  in  1854  and  its  contagiousness  was  experimentally 
shown  by  Gerlach.  In  1850,  Heusinger  published  a  very 
comprehensive  treatise  on  anthrax  which  deals  at  length  with 
its  history  and  geographical  distribution. 

Much  new  information  concerning  the  nature  of  anthrax 
was    acquired    during    the    fifth    decade  of  the  last    century. 

In  1S55,  Pollander  an- 
nounced the  discovery, 
which  he  first  made 
in  1849,  of  minute 
uubranched  rod-shaped 
bodies  in  the  blood  of 
cattle  dead  of  anthrax. 
Davaine  observed  simi- 
lar  bodies  in  1850. 
Then  followed  a  long 
series  of  observations 
and  somewhat  contro- 
versial discussions  on 
the  bacterial  origin  of 
the  disease,  culminat- 
ing by  Robert  Koch's 
careful  description  of 
the  morphology  of  its 
specific  organism  including  the  spore  formation  in  1876 
(1877  Pasteur).  Cohn,  however,  seems  to  have  been  the  first 
to  have  called  the  organism  a  Bacillus  and  to  have  suspected 
the  existence  of  spores.  Toussaint,  in  1880,  and  Pasteur  in 
188 1,  published  results  of  investigations  directed  toward  pro- 
tective inoculation.  Since  that  time,  the  literature  on  the 
cause,  morbid  anatomy  and  prevention  of  anthrax  has  become 
very  extensive. 


Fig.  21.  Anthrax  bacteria  in  an  im- 
pression preparation  made  from  a  colony 
on  an  agar  plate  culture. 


ETIOLOGY  131 

§  118.  Geographical  distribution.  Anthrax  is  a  widel}- 
disseminated  disease.  The  continent  of  Europe  has  perhaps 
suffered  most  from  its  ravages.  It  occurs,  also,  in  Northern, 
Eastern  and  Central  Africa,  where  in  recent  years  it  has 
become  a  great  plague.  In  Siberia,  it  has  caused  fearful  des- 
truction, and  in  that  country  it  is  still  known  as  the  "Siberian 
Plague."  It  has  frequently  appeared  in  England.  Russia, 
India  and  Australia  are  also  infected.  South  America  is  also 
reported  to  suffer  much  from  its  ravages.  In  the  United  States 
it  has  been  reported  from  at  least  fifteen  states.  In  fact  there 
are  very  few,  if  any,  countries  where  this  disease  has  not  been 
found.  A  knowledge  of  its  specific  cause,  with  the  methods 
of  properly  disposing  of  dead  animals,  isolation  and  disinfec- 
tion, as  well  as  the  preventive  inoculations  now  in  vogue,  have 
made  it  possible  to  prevent  wide-spread  epizootics.  In 
America  it  is  looked  upon  as  a  comparatively  rare  disease, 
excepting  in  certain  infected  districts. 

§  iig/  Etiology.  Anthrax  is  due  to  the  presence  of  a 
microorganism  known  as  Badermm  anthracis.  This  organism 
is  found  in  the  diseased  tissues  and  organs  of  affected  animals. 
On  account  of  its  spores,  it  is  very  resistant  to  the  normal 
destructive  agencies  in  nature.  Consequently  when  it  is  once 
introduced  into  a  locality  it  tends  to  remain  there  for  many 
years,  possibly  causing  from  time  to  time  a  few  cases  of  anthrax 
or  serious  epizootics  or  epidemics.  The  spores  are  also  fre- 
quently carried  in  the  wool,  hair,  hides,  hoofs  and  horns  taken 
from  animals  sick  or  dead  of  anthrax.  Thus  the  affection  has 
been  introduced  into  far  distant  localities. 

Bacterium  anthracis  is  a  rod-shaped  organism  varying  in 
length  from  i  to  4  /i,  but  having  a  quite  uniform  breadth  of 
about  one  micron.  In  a  suitable  medium  it  grows  out  in  long 
flexible  filaments  which  combine  to  form  thread-like  bundles. 
When  examined,  the  ends  of  the  rod  seem  to  be  square  cut. 
In  preparations  from  animal  tissues  there  appear  sometimes  to 
be  slight  concavities  in  the  ends  of  the  segments  when  two  of 
them  are  united.     In  cultures  spores  are   formed.     These  are 


132  ANTHRAX 

oval,     highly    refractive    bodies    held    within    the     cellular 
envelopes  of  the  filaments,  but  later  they   are   set  free  by  the 


Fig.  22.     Anthrax  bacteria   in    a   cover-glass   preparation   of  blood 
sho-u'ing  chains  and  capsules. 

dissolution  of  this  membrane.     They    stain    readily    with    the 
aniline  dyes  and  also  b}^  Gram's  method. 

The  bacterium  of  anthrax  itself  is  not  an  especially  hardy 
organism.  On  the  contrary  it  is  easily  destroyed  by  weak 
disinfectants  and  it  has  a  low  thermal  death  point.  Its  spores, 
however,  are  among  the  most  hardy  of  bacterial  life  to  resist 
chemical  and  thermal  agents.  They  resist  drying  for  months 
or  years  and  often  boiling  for  a  half-hour  or  longer  does  not 
destroy  them.  On  this  account  it  is  very  difiicult  to  eliminate 
the  virus  from  infected  pasture  lands,  especially  if  they  are 
wet  or  marshy. 

As  the  spores  may  remain  on  the  soil  in  a  dormant  condi- 
tion for  many  years,  it  sometimes  happens  that  the  disease 
does  not  appear  until  long  after  the  introduction  of  the  virus. 
Anthrax  has  been  known  to  break  out  among  cattle  grazing 
on  a  field  in  which  the  carcasses  or  hides  from  affected  animals 
were  buried  many  years  before.  Through  some  means  the 
spores  seem  to  be  able  to  get  to  the  surface  and  contaminate 
the  grass.     The  virus  may  be  introduced   with   blood  or  bone 


CHANNELS    OF    INFECTION  133 

fertilizers,  hides,  hair  or  wool  from  infected  countries.  When 
the  extent  of  this  traffic  is  realized,  it  is  easy  to  understand 
how  anthrax  has  been  brought  to  this  country  and  whj'  it 
occasionally  appears  here  and  there  over  a  large  part  of  the 
continent.  Many  outbreaks,  as  well  as  isolated  cases,  illustrat- 
ing this  common  method  of  dissemination  are  on  record. 

The  period  of  incubaf ion  \s  \Qry  s\\or\..  In  inoculated  ani- 
mals it  ranges  from  i  to  5  days. 

§  120.  Animals  attacked.  Nearly  all  species  of  ani- 
mals suffer  from  anthrax.  The  herbivora  and  rodents  are 
most  susceptible.  Horses  and  mules  often  suffer  from  it. 
M'Fadyean  has  reported  outbreaks  aggregating  54  cases,  of 
which  49  were  cattle,  4  horses  and  i  pig.  He  states  also  that 
for  a  period  of  5  years  there  had  been  reported  192  cases  in 
horses  and  3,390  in  cattle.  It  is  interesting  to  note  that  the 
Algerian  race  of  sheep  are  immune.  A  satisfactorj'  explana- 
tion for  this  striking  exception  has  not  been  recorded.  It  has 
been  stated  that  a  single  bacterium  introduced  into  the  subcu- 
taneous connective  tissue  of  a  guinea  pig  or  mouse  is  sufficient 
to  kill  it.  Cats,  tame  and  wild  rabbits  and  hares  are  the  next 
most  susceptible  species.  It  is  stated  that  dogs,  pigs  and  foxes 
are  very  slightly  susceptible.  Rats,  fowls  and  pigeons  are 
reported  to  be  immune.  Fish  and  amphibia  are  rarely 
attacked. 

^  121.  Channels  of  infection.  Three  common  modes 
of  infection  are  recognized  for  anthrax,  namely  :  through  the 
digestive  tract,  by  the  skin  and  by  the  lungs.  In  cattle  the 
infection  seems  to  be  largely  through  the  alimentary  canal  ; 
in  horses  and  sheep  by  the  skin  or  digestive  tract  ;  in  men 
through  wounds  of  the  skin  and  the  respiratory  tract. 
Although  these  are  the  usual  methods  there  are  many  excep- 
tions with  each  species. 

I.  Infection  througli  t/ie  alimentary  canal.  This  is  the 
more  common  mode  of  infection  in  cattle.  The  resulting 
disease  has  been  designated  by  various  names,  among  which 
are    "intestinal   anthrax,"    "fodder  anthrax,"    "spontaneous 


134  ANTHRAX 

anthrax,"  internal  anthrax,"  "anthrax  fever,"  and  anthrax 
without  external  manifestations.  In  these  cases  the  infecting 
organisms,  either  the  spores  or  the  vegetating  bacteria  them- 
selves, are  taken  into  the  body  with  food  or  drinking  water. 
M'Fadyean  has  recently  shown  that  infected  food  stuffs  are 
often  responsible  for  the  infection.  It  is  stated  that  the 
infection  takes  place  in  most  cases  in  the  small  intestine,  the 
mucosa  of  which,  it  is  stated,  need  not  necessarily  be  injured. 
It  is  highh'  probable  that  the  gastric  juice  destroys  most  of  the 
bacteria  while  the  free  spores  are  not  injuriously  affected  by 
it.  In  the  infected  districts,  the  spores  exist  at  or  upon  the 
surface  of  the  soil  and  possibly  on  the  blades  of  grass,  from 
which  they  are  easily  taken  up  by  grazing  animals.  In  lands 
thus  infected,  the  specific  organism  has  been  introduced  at 
some  previous  time  either  by  the  burying  of  anthrax  animals 
in  these  fields,  by  the  use  of  infected  tannery  or  slaughter 
house  refuse  as  fertilizers,  by  flooding  from  infected  streams, 
or  by  the  bringing  of  the  organism  in  the  droppings  of  birds 
or  other  small  animals  which  have  fed  upon  anthrax  carcasses. 
It  is  reported  that  the  spores  will  find  their  way  to  the  surface 
even  when  the  dead  animals  have  been  buried  at  a  considerable 
depth.  There  has  been  some  controversy  in  the  writings  of 
Pasteur,  Koch  and  Bollinger  concerning  the  method  by  which 
the  spores  reach  the  surface.  Pasteur  supposed  that  they  were 
brought  by  earth  worms  from  the  buried  carcasses.  Koch 
believed  this  impossible  because  of  the  low  temperature  of  the 
ground  at  the  depth  at  which  the  animals  are  buried.  Bol- 
linger has  shown  experimentally  the  possibility  of  Pasteur's 
views.  Karliniski  and  others  have  found  that  the  spores  of 
anthrax  may  be  disseminated  by  slugs,  insects  and  larvae 
which  are  found  on  untanned  infected  skins. 

2.  Infection  through  the  skin.  In  animals,  this  mode  of 
infection  occurs  less  frequently  than  in  man.  Anthrax  pro- 
duced in  this  way  is  usually  characterized  by  local  manifesta- 
tions known  as  "carbuncle  disease,"  or  "malignant  pustule." 
In  this  mode  of  infection  the  bacteria  penetrate  through 
wounds  in  the  skin  and  exposed   mucous  membranes  into  the 


SYINIPTOMS  135 


living  tissues  by  means  of  infected  utensils,  the  use  of  infected 
instruments,  and  insects,  especially  the  house  fly  {Miisca 
domestua.)  Dalrymple  has  called  attention  to  the  spread  of 
this  disease  among  animals  in  the  lower  Mississippi  Valley 
by  means  of  the  horse  fly  (^Tabanidae).  In  man  many  cases 
of  the  disease  occur  from  the  injuries  or  cuts  made  at  the  post- 
mortem of  anthrax  animals  or  by  the  infection  of  skin  wounds 
while  handling  infected  hides  or  wool.  Malignant  pustule  is 
reported  to  be  quite  common  among  the  employes  of  certain 
tanneries  and  upholstering  establishments  where  hides  and 
hair  imported  from  infected  districts  or  countries  are   used. 

3.  Infection  through  the  respiratory  tract.  Faser,  Buch- 
ner,  Lemke,  and  other  writers  have  shown  experimentally 
that  the  disease  can  be  produced  by  the  inhalation  of  spores. 
In  man  this  form  of  infection  is  quite  common  among  the  wool 
sorters.  In  Great  Britain,  where  much  foreign  wool  is  handled, 
it  has  been  reported  as  causing  as  many  as  500  deaths 
annually.     It  is  known  as  "wool-sorters'  disease." 

§  122.  Symptoms.  In  anthrax,  the  symptoms  vary 
not  only  in  different  species  of  animals  but  also  in  diff"erent 
individuals  according  to  the  location  of  the  disease.  Again 
there  is  often  considerable  variation  when  the  lesions  are 
apparently  the  same.  The  most  characteristic  features  of  the 
disease  are  the  suddenness  of  the  attack,  the  grave  general 
disturbances,  high  elevation  of  temperature,  a  tendency  to 
ecchymosesofthe  mucous  membranes  and  local  manifestations, 
such  as  carbuncles  and  edema  of  the  skin,  digestive  disturb- 
ances, brain  complications  and  difficult  respiration. 

Anthrax  has  been  classified  according  to  its  course  as  per- 
acute,  acute  and  subacute.  It  has  also  been  divided  accord- 
ing to  the  site  of  its  manifestations  as  anthrax  with  visible 
localization  and  anthrax  without  visible  localization. 

Anthrax  zvithout  visible  localization.  This  form  is  gener- 
ally due  to  ordinary  infection  presumably  by  spores.  It 
includes  the  peracute,  acute,  and  subacute. 

I.     The   peracute    or    apoplectic    anthrax    gives    rise    to 


136  ANTHRAX 

symptoms  of  cerebral  apoplexy.  The  animal  becomes  sud- 
denly ill,  staggers  about  for  a  brief  period  and  falls.  There  is 
often  a  bloody  discharge  from  the  mouth,  nostrils  and  anus. 
Death  usually  ensues  in  from  a   few    minutes    to    an    hour. 


/ 


<^ 


/ 


Fig.    23.     A  camera  Iiicida  drazcitig  of  a  field  in    a   preparation    of 
blood  from  a  case  of  acute  anlhrax ,  much  enlarged  {Burnett). 

Usually  there  are  convulsions.  Sheep  and  cattle  suffer  most 
frequently  with  this  form  of  the  disease.  They  are  often 
found  dead.  This  is  especially  true  in  the  beginning  of  an 
epizootic. 

2.  In  the  acute  form,  the  disease  runs  a  somewhat  slower 
course,  lasting  usually  not  to  exceed  twenty- four  hours.  The 
temperature  rises  rapidly  to  from  105  to  108°  F.  With  this 
there  are  signs  either  of  congestion  of  the  brain  or  of  the 
lungs.  If  the  brain  is  affected  the  animal  becomes  restless, 
excited,  stamps  the  ground,  rears  in  the  air,   bellows,  runs  to 


SYMPTOMS  137 

and  fro  and  finally  goes  into  convulsions  followed  by  stupor 
and  death.  If  the  lungs  are  congested  there  is  difficulty  in 
breathing,  more  or  less  wheezing,  panting,  groaning,  palpita- 
tion of  the  heart,  small  and  frequent  pulse,  cyanosis  of  the 
mucosaof  the  head,  bloody  discharges,  hematuria,  staggering 
and  finally  convulsions  and  death  from  suffocation.  Occasion- 
ally there  is  a  partial  remission  of  the  symptoms,  followed  by 
relapse.  It  has  been  observed  that  occasionally  there  are  pre- 
monitory symptoms  preceding  the  acute  attack,  consisting  of 
slight  digestive  disturbances  and  diminished  vivacity.  Burnett 
found  the  anthrax  bacteria  in  large  numbers  in  the  blood  dur- 
ing this  stage.  He  likewise  found  them  to  be  present  in  the 
blood  of  the  more  chronic  cases  during  the  febrile  period. 

3.  The  subacute  form  is  known  as  anthrax  fever  or 
intermittent  anthrax.  The  symptoms  are  the  same  as  in  the 
other  forms,  except  that  they  are  more  sharply  defined  and  the 
course  is  longer.  The  disease  lasts  from  one  to  seven  or  eight 
days,  the  average  being  about  forty-eight  hours.  The  high 
temperature,  the  congestion  of  the  lungs  or  brain  complicated 
with  intestinal  disturbances,  especially  colic,  are  usually  well 
marked.  In  epizootics  where  the  peracute  or  acute  form 
ushers  in  the  disease,  the  later  cases  usually  are  of  the  sub- 
acute variety. 

Anthrax  icith  visible  localisation.  These  forms  usually 
result  from  infection  of  the  skin  and  mucous  membranes. 
The  lesions  are  spoken  of  as  carbuncles  and  often  there  is 
marked  local  edema  of  the  skin.  This  form  is  common  in 
manv  horses  and  sometimes  it  occurs  in  cattle.  It  is  reported 
to  occur  in  other  species.  The  carbuncles  are  circumscribed, 
cutaneous  swellings  which  are  at  first  hard,  hot  and  painful. 
Later  they  become  cold  and  painless,  with  a  tendency  to 
become  gangrenous.  The  edematous  tissue  becomes  doughy, 
cold  to  the  touch  and  painless.  Frequently  fluctuating  swell- 
ings of  the  skin  occur.  The  duration  of  this  form  of  the  dis- 
ease varies  from  four  to  fifteen  days.  Ordinarily  it  is  not  so 
fatal  as  internal  anthrax. 

When    the    infection    is   on    the    mucous    membrane    the 


138  ANTHRAX 

animal  suffers  from  fever,  dyspnea,  difficulty  in  swallowing- 
and  cyanosis,  together  with  the  immediate  local  effects. 
Death  occurs  much  sooner  than  when  the  disease  is  located  on 
the  skin.  It  is  stated  that  dogs  and  swine  suffer  from  this 
form  more  than  from  the  acute  types. 

In  horses,  anthrax  usually  runs  an  acute  or  subacute 
course.  The  first  symptom  is  rise  of  temperature  with  a  rapid, 
feeble  pulse.  There  may  be  chills  and  muscular  spasms. 
The  mucosa  of  the  head  becomes  cyanotic  and  lacrymation  is 
often  present.  The  animal  has  a  dull,  stupid  look,  appears  to 
be  stunned  and  walks  with  a  staggering  gait.  In  some  cases 
there  are  symptoms  of  cerebral  congestion,  such  as  restlessness 
or  convulsions.  Colic  is  a  very  characteristic  symptom  in  the 
horse,  otherwise  the  symptoms  are  the  same  as  in  cattle. 
Infection  of  the  skin  usually  occurs  on  the  hypogastrium, 
lower  part  of  the  breast,  inner  surface  of  the  fore  and  hind 
quarters.  Swelling  of  the  hind  quarters  often  causes  lameness. 
Carbuncles  of  the  mucous  membrane  of  the  tongue  are  said  to 
be  rare  in  this  species. 

In  sheep  and  goats  the  disease  is  usually  of  the  acute  or 
apoplectic  form.  The  animals  appear  as  if  suddenly  stricken 
with  apoplexy.  If  death  does  not  occur  within  a  very  short 
time,  symptoms  already  described  for  this  form  of  the  disease 
may  be  recognized.  Subacute  anthrax  is  said  to  be  very  rare 
in  sheep. 

In  swine,  anthrax  is  ordinarily  characterized  by  local 
lesions  on  the  mucous  membrane  of  the  larynx  and  pharynx. 
The  animals  have  a  rise  of  temperature  and  the  intermaxillary 
space  is  generally  swollen.  The  swelling  may  spread  along 
the  trachea,  giving  rise  to  difficulty  in  swallowing,  hoarseness, 
cyanosis  of  the  mucosa  of  the  mouth,  dyspnea  and  rapid 
breathing.  The  animal  shows  signs  of  paralysis.  Death 
occurs  from  suffocation.  Frequently  the  tongue  becomes  the 
seat  of  the  disease.  Carbuncles  occurring  on  the  skin, 
especially  of  the  back,  have  been  described  in  this  species. 

In  dogs  and  cats,  the  disease  usually  rans  a  very  rapid 
course.     The  fact  that  they  are  usually  infected  by  eating  the 


MORBID    ANATOMY  ^39 

meat  of  animals  dead  of  anthrax  causes  them  to  suffer  largely 
from  the  intestinal  form.  It  has  been  stated  that  probably 
much  of  the  so-called  anthrax  in  dogs  is  simply  cases  of 
ptomaine  poisoning. 

It  is  reported  that  in  birds  anthrax  usually  runs  a  very 
rapid  and  usually  fatal  course.  Toward  the  end  they  stagger, 
tremble  or  go  into  convulsions  and  die  with  bloody  discharges 
from  the  mouth,  nostrils  and  anus.  From  the  first  the  birds 
are  depressed,  weak,  and  their  feathers  ruffled.  There  is 
evidence  of  dyspnea.  Carbuncles  are  said  to  appear  on  the 
comb,  wattles,  conjunctiva,  tongue  and  extremities. 

It  has  been  stated  that  the  milk  from  cows  suffering  with 
anthrax  contains  Bad.  anthracis.  The  writer  found  in  the 
examinations  made  in  one  epizootic  that  the  anthrax  bacteria 
were  present  in  considerable  numbers  in  the  milk  just  before 
or  immediately  after  death,  but  they  were  not  found  in  the 
milk  of  animals  in  the  earlier  stages  of  the  disease. 

§123.  Morbid  anatomy.  The  nature  and  extent  of  the 
tissue  changes  depend  upon  the  course  of  the  disease.  When 
experimentally  produced  it  is  ordinarily  a  septicemia.  This 
form  often  occurs  in  domesticated  animals  when  they  contract 
the  disease  naturally.  The  more  common  anatomical  changes 
except  in  the  most  acute  cases  and  in  the  strictly  localized 
lesions  or  carbuncles,  are  : 

Hemorrhages  varying  in  amount  from  petechiae  to  blood 
extravasations,  with  more  or  less  .serous,  gelatinous  and  hem- 
orrhagic infiltration  of  the  submucous,  subserous  and  subcuta- 
neous tissue. 

The  capillaries  are  distended  and  frequently  there  are 
hemorrhages  beneath  the  epidermis.  The  subcutis  is  spnnkled 
with  ecchymoses.  Frequently  there  are  gelatinous  effusions 
of  a  rather  firm  consistency  and  of  varying  size.  The  color 
also  differs,  ranging  between  a  deep  yellow  and  a  yellowish 
brown.  Often  these  edematous  areas  are  spnnkled  with  hem- 
orrhagic foci.     A  simple  serous  edema  may  occur. 

The  lymphatic  glands   may    be   hemorrhagic,    edematous 


I40  ANTHRAX 

or  both.  An  edema  of  the  connective  tissues  of  the  neck  or 
about  the  trachea  is  often  ver}'  marked. 

The  muscles  vary  in  color  but  usually  they  are  darker 
than  normal,  and  like  the  skin,  they  often  become  sprinkled 
with  ecchymoses.  The  heart  muscle  suffers  from  parenchy- 
matous changes. 

In  the  larger  cavities  of  the  body,  a  sanguinolent  fluid  is 
found  in  moderate  quantities.  Blood  extravasations  of  differ- 
ent sizes  are  seen  under  the  serous  membranes,  particularly  on 
the  mesentery  and  mediastinum.  The  subserous  connective 
tissue,  especially  on  the  mesentery,  anterior  mediastinum  and 
in  the  neighborhood  of  the  kidneys,  is  often  infiltrated  with  a 
gelatinous  substance.  On  this  account  the  neighboring  lymph 
glands  are  considerably  swollen,  filled  with  serum  and 
sprinkled  with  hemorrhages.  The  internal  organs  contain  a 
large  quantity  of  blood.  All  the  larger  veins  and  the  heart 
are  filled,  while  the  surrounding  tissues  show  sanious 
imbibition. 

The  spleen  is  usually  considerably  enlarged  (two  to  five 
times  its  normal  size),  either  uniformly  or  by  prominent 
tumor-like  protuberances.  The  pulp  is  soft,  more  or  less  fluid, 
and  stained  a  dark  red  color.  The  capsule  is  always  very 
tense.  It  is  frequently  sprinkled  with  ecchymoses.  Occasion- 
ally this  organ  is  slightly  affected. 

The  liver  and  kidneys  are  highly  congested  and  some- 
what enlarged.  The  parenchyma  contains  areas  of  blood 
infiltration  and  the  cells  themselves  manifest  various  kinds  of 
degeneration.  The  portal  lymph  glands  often  appear  to  be 
enlarged,  and  the  retroperitoneal  tissue  may  be  infiltrated  with 
a  serous,  gelatinous  fluid.  The  subperitoneal  tissue  of  the 
intestines  and  of  the  abdominal  walls  may  be  similarly 
affected. 

The  nature  of  the  lesions  of  the  intestinal  canal  varies 
according  as  the  disease  is  intestinal  anthrax,  or  anthrax 
caused  by  inoculation.  In  case  of  inoculation  anthrax,  the 
intestine  is  frequently  normal.  In  other  cases  there  may  be 
submucous   and  subserous    hemorrhages,  or   swelling   of  the 


MORBID    ANATOMY  I4I 

mesenteric  glands.  The  principal  changes  in  intestinal  an- 
thrax are  always  found  in  the  small  intestine,  chiefly  in  the 
duodenum.  In  the  milder  cases  of  intestinal  anthrax  the 
mucous  membrane  is  affected  by  circumscribed  or  diffuse 
swellings.  The  bacteria  are  often  found  in  very  large  num- 
bers on  the  surface  of  the  raucous  membrane.  Necroses  and 
ulcers  appear  in  those  parts  where  the  bacteria  are  most 
thickly  congregated.  In  very  severe  cases,  the  abomasum  or 
the  true  stomach  may  be  affected  with  a  gelatinous  and  sanious 
infiltration  of  the  mucous  membrane.  The  mucosa  of  the 
abomasum,  and  especially  of  the  duodenum,  is,  in  consequence 
of  excessive  hyperemia,  dark  red  or  almost  black,  and  is 
covered  with  ero.sions  and  ulcers  or  necroses,  which  may 
extend  down  to  the  submucosa.  The  contents  of  the  intestine 
are  bloody,  and  the  submucosa  is  infiltrated  with  a  serous, 
gelatinous,  or  hemorrhagic  exudate,  so  that  the  mucous  mem- 
brane often  projects,  in  the  form  of  large  tumors,  into  the 
lumen  of  the  intestine.  On  the  site  of  Peyer's  patches  and  the 
solitary  follicles  we  may  find  flat  or  prominent  nodules,  the 
surface  of  which  are  covered  with  diphtheritic  crusts. 

The  lungs  are  greatly  congested,  edematous  and  show 
areas  of  ecchymoses.  The  entire  respiratory  mucous  mem- 
brane is  considerably  reddened  and  ecchymotic.  The  mucous 
membrane  of  the  pharynx  and  opening  of  the  larynx  is  often 
so  edematous  that  stenosis  of  the  larynx  takes  place.  The 
contents  of  the  trachea  and  the  bronchi  consist  mostly  of 
bloody  froth  or  mucus. 

The  brain  is  often  studded  with  ecchymoses.  The  sur- 
face of  its  membranes  often  exhibits  hemorrhages  with  an 
accumulation  of  sanious  serum  in  the  ventricles.  Extravasa- 
tions of  blood  sometimes  occur  in  the  anterior  chamber  of  the 
eye  and  under  the  retina.  All  the  other  organs  may  contain 
hemorrhages,  and  the  urine  frequently  contains  blood. 

The  blood  is  usually  dark.  It  has  a  tarry  or  varnish- like 
lustre,  and  shows  little  tendency  to  coagulate.  It  does  not 
assume  its  normal  red  color  when  exposed  to  the  air.  Burnett 
studied  the  blood  ot  a  few  cases  of  anthrax  in  1904.  The 
appended  tables  are  taken  from  the  results  of  his  examinations. 


142 


ANTHRAX 


RESULT   OF   THE   EXAMINATION   OF   THE   BLOOD   OF    FIVE   CASES   OF 
ANTHRAX  IN   CATTLE. 


1      First         Date  of         S^ 

Cow       .symptom       Exam-         2"  = 

1  observed      ination         S  s 

Hemo- 
globin 
per 
cent. 

Red 
Corpuscles 
per  c.  mm. 

Leuco- 
cytes 
per 
c.  mm. 

Remarks 

No.    8  Ijuly    8                     107.5° 

Anth.  bact.i 
in  blood 

I 

"      8                      Jul.v    9     106.6 

60 

4,072,000 

20,000 

Died  July  9 

"      4*  July  ID                      106.2 

"      4                     July  II 

56 

5,471,000 

4,814 

"      4                         "     13     103.0 

38 

3,400,000 

3,444 

"      4                         "     19 

56 

2,086,000 

9,876 

Recovered 

"      6tJuly    7 

"      6  '                  July    9     104.0 

50 

3,876,600 

8,222 

Anth.  bact. 
in  blood 

"      6  ;                      "     II 

60 

3,954,000 

5,210 

,"      6                         '•     13 

101.8 

"      6 

"     14 

101.2 

47 

3,484,000 

5,666 

Apparently 

recovered. 

Died  of 

Anthrax 

Nov.  4 

"      6 

"     19 

54 

I ,980,000 

8,777 

"      6 
"      3 

"     24 

63 

3.132,000 

11,888 

June  29 

July  14 

101.2 

57 

4,168,000 

5,222 

Recovered  | 

"      I    July  15 

1 

July  16 

103.8 

53 

2,324,000 

8,111                         1 

"     17 

lOI.O 

58 

2,632,000 

5,333 

"     18    102.0 

8,163 

"     ^^i 

5,940,000 

11,000 

61 

10,767 

Recovered  ' 

1 

1                              ! 

*Teraperature  July  8,  102.1°. 
iTemperature  Julys,  107.4°. 


Temperature  July  10,  100.0°. 
Temperature  July  9,  103.0°. 


^lORBID    ANATOMY 


143 


THE    DIFFRRKNTIAf,   COtTNT  OF   THE    LEUCOCYTES     IN     FIVE     CASKS 
ANTHRAX    IN    CATTI^E. 


COW 

Date 

I^ympho. 
cytes 

Large  Mono 
nuclear 

Polynuc- 
lear 

Eos 
phi 

Ho- 
les 

Masst 
Cells 

No. 

0/ 

No. 

% 

No.     % 

No. 

I 

No. 

.?! 

48 
7 
II 

0.4 
0.2 

I.O 

0.2 
0.2 

0.5 

°:! 
0.7 

I.I 

0.4 

0.7 

0.2 

0.8 
0.7 

0.5 

Soper 
No.  8 

1   "    4 

July  9  20000 

7080 

35-4 

2200 

II.O 

7120  35.6 

3520 

548 

75 

636 

17.6 

2.8 

II. 4 
2.2 

6.4 

"     11!  4S14 

1670 

27.4 

5-2 

|64.8 

1   ,,     ,, 

t 

i   "     " 

34.7 

341 

7-1 

2200I  45-7 

"     13 

3444 

1432 

41.6 

261 

7.6 

i667|  48.4 

"     19 

9876 

4257 

43-1 

273 

2.7 

4696  47-5 

"    ^ 

"      9    8222 
"    ii;  5210 

3930 
2287 

47.8 
43  9 

296 

3-6 

3436  41.8 

518 

6.3 

41 
36 

62 

35 

I9 

10 

65 
36 

55 
86 

"     " 

338 

65 

2115!  40.6 

432  i    8.3 

"    " 

"    13 

40.1 

40 

47.2 

7.8 

..    <. 

"    14   5666 

2833    50.0 

119 

2.1 

2221   39.2 

430;     7-6 
[930  22  0 

~77~7r 

"    19   8777 
"    2411S88 

3747    42.7 

263 

3-0 

2800  31.9 

6033    50.7 

698 

5-8 

3120  26.2 

1946 
146 

1330 
640 
734 

16.3 
2.8 

16.4 
12.0 
9.0 

"    3 

"    14I  5222 

3352    64.2 

261 

5-0 

1451   27.8 

Bradish 
No.  I 

1 
"     16    8rii 

35281   43-5 

154 

1-9 

3033'  37-4 

[   .<     <. 

"     17    5333 
"     18,  8163 

2832    53-1 

256 

4.8 

1368:  29.4 

t   ".  " 

6375    78.1 

138 

1-7 

914 

II. 2 

"     '« 

"     i9|iiooo 

661 1    60.1 

253 

2.3 

2585 

23-5 

1496,  13.6 

1   "     " 

"    2410767 

5911    54-9 

484 

4-5 

2186 

.0.3 

2099 

.9.5 

He  found  that  the  number  of  red  corpuscles  and  the  per- 
centage of  hemoglobin  are  reduced.  In  the  chronic  cases 
they  tend  to  return  to  the  normal  condition.  There  was  an 
increase  in  the  number  of  lymphocytes  and  a  decrease  in  the 
number  of  polynuclear  leucocytes.     In  some  cases  there  was  a 


144  ANTHRAX 

marked  increased  in  the  number  of  eosinophiles.  No  change 
from  the  normal  was  noted  in  the  large  mononuclear  leuco- 
cytes or  in  the  mast  cells. 

The  bodies  of  animals  which  have  died  from  anthrax  aie 
often  well  nourished.  Rigor  mortis  is  absent  and  they  decom- 
pose quickly.  Very  frequently  blood  flows  from  the  natural 
openings  of  the  body,  and  the  rectum  is  sometimes  prolapsed. 

All  the  foregoing  lesions  may  be  absent  in  very  acute 
apoplectic  cases.  The  specific  organism  is,  however,  always 
present  in  the  cadaver.  It  is  important  to  note  that  occasion- 
ally the  usual  changes  indicated  by  the  symptoms  and  the  dur- 
ation of  the  disease  are  not  found  on  post-mortem  examination. 
In  one  epizootic,  the  writer  saw  an  animal  dead  from  subacute 
anthrax  in  which  the  blood  and  tissues  were  teeming  with 
anthrax  bacteria,  yet  the  organs  examined  macroscopically 
appeared  to  be  normal.  Other  animals  in  the  same  outbreak 
exhibited  the  more  usual  anatomical  changes. 

The  period  of  dtiration  varies  from  a  few  hours  to  a  week 
or  even  longer. 

The  prognosis  is  unfavorable.  In  some  herds  the  mor- 
tality is  ICO  per  cent  while  in  others  a  number  of  animals 
may  recover.  The  average  mortality  is  placed  at  about  70 
per  cent  in  animals.  In  the  human  species  many  persons 
recover  from  its  local  form  (malignant  pustule). 

M'Fadyean  has  reported  this  disease  in  39  consecutive 
outbreaks  in  which  a  total  of  54  animals  died.  In  New  York 
the  disease  existed  in  1904  in  15  herds  in  one  locality.  There 
were  more  than  30  deaths.  In  one  herd  of  21  animals,  20  had 
the  disea.se,  16  died  and  4  recovered.  In  another  dairy  4  out 
of  7  died,  but  in  the  others  one  or  two  animals  in  each  was 
affected.  In  1906  anthrax  occurred  on  84  different  farms  in 
the  same  county.  There  were  170  fatal  cases  of  which  2>c> 
were  in  horses,  123  in  cattle,  11  in  sheep,  and  3  in  hogs 
(Burnett).  These  facts  are  interesting  in  showing  that  the 
disease  does  not  always  cause  heavy  losses  in  the  infected 
herds. 


DIFFERENTIAL   DIAGNOSIS  I45 

§  124.  Differential  diagnosis.  It  is  important  not  to 
confuse  anthrax  with  a  number  of  non-specific  disorders  and 
accidental  causes  of  death.  The  suddenness  of  the  attack,  and 
in  very  virulent  cases,  the  short  duration  of  the  disease  may 
tend  to  the  mistaking  of  it  for  poisoning,  cerebral  apoplexy, 
pulmonary  congestion,  heat  apoplexy,  death  from  lightning,  or 
acute  gastro-intestinal  inflammation.  The  affection  known  as 
corn-stalk  disease  is  not  infrequently  taken  for  anthrax  and 
vice  versa.  In  all  of  these  cases  the  doubt  following  the  post- 
mortem can  be  easily  settled  by  a  bacteriological  examination 
which,  with  genuine  anthrax,  will  reveal  the  presence  of  Bac- 
terium anthracis.  It  is  believed  by  those  who  have  dealt  most 
with  anthrax,  that  the  specific  organisms  are  always  in  the 
circulating  blood  before  death.  The  putrefactive  organisms 
that  resemble  Bacterium  anthracis  morphologically  do  not 
appear  in  the  cutaneous  blood  as  quickly  after  death  as  they 
do  in  the  organs. 

There  are,  however,  certain  specific  diseases  from  which 
anthrax  must  be  differentiated.  The  most  important  of  these 
are  symptomatic  anthrax  (black  leg),  malignant  edema,  and 
septicemia  hemorrhagica.  Rabies  is  not  infrequently  taken 
for  anthrax.  If  the  diagnosis  cannot  be  determined  by  the 
anatomical  changes  (which  can  be  relied  upon  only  in  some- 
what typical  cases)  the  positive  diagnosis  can  be  made  only 
with  the  finding  of  the  anthrax  bacteria.  In  animals  just 
dead,  where  decomposition  has  not  begun,  these  organisms  can 
usually  be  found  in  properly  stained  cover-glass  preparations 
made  directly  from  the  blood  or  ti.ssues.  After  decomposition 
begins  to  take  place,  a  putrefactive  organism,  that  is  not  easily 
distinguished  from  that  of  anthrax,  often  appears  in  the  tissues. 
It  is,  therefore,  necessary  in  such  cases  to  resort  to  culture 
methods  before  a  positive  statement  can  be  made.  As  the 
bacilli  of  malignant  edema  and  symptomatic  anthrax  are 
anaerobes,  they  will  not  develop  in  aerobic  cultures,  such  as 
on  slant  agar  or  in  bouillon.  The  bacterium  of  .septicemia 
hemorrhagica,  being  a  small  oval  organism,  is  easily  told 
from  that  of  anthrax.      It  is  important  to  recognize  the   possi- 


146  ANTHRAX 

bility  of  error,  if  the  conditions  restrict  the  examination  to  the 
study  of  the  microscopic  preparations. 

Differential  stain.  M'Fadyean  has  described  a  peculiar 
staining  reaction,  first  pointed  out  by  Heins,  which  he  con- 
siders of  value  for  the  microscopic  diagnosis  of  this  disease. 
The  reaction  is  in  evidence  when  films  of  blood,  exudates,  or 
tissue  juice  containing  the  bacteria  are  stained  with  a  simple 
aqueous  solution  of  methylene  blue.  The  method  as  applied 
to  blood  is  as  follows  : 

Place  a  drop  of  the  blood  on  a  clean  slide.  The  size  of 
the  drop  should  be  about  2  mm.  in  diameter.  It  is  spread 
quickly  with  a  platinum  needle  until  it  covers  an  area  about 
12  mm.  in  diameter.  Protect  from  dust  and  allow  the  slide  to 
remain  until  all  evidence  of  moisture  has  disappeared.  When 
dry,  heat  the  preparation  by  lowering  it  film  upwards  into  the 
flame  of  a  Bunsen  burner  or  an  alcohol  lamp  for  a  second. 
Repeat  this  three  times  or  until  the  glass  is  too  hot  to  be  borne 
by  the  skin  in  the  palm  of  the  hand.  Allow  the  slide  to  cool 
and  then  cover  the  film  with  i  per  cent  aqueous  solution  of 
methylene  blue.  After  a  few  seconds  pour  ofi^  the  free  stain 
and  wash  the  slide  thoroughly  in  tap  water.  Dry  the  slide  by 
pressing  it  gently  between  two  layers  of  bibulous  paper,  and 
then  more  thoroughly  by  holding  it  in  the  current  of  hot  air 
above  the  Bunsen  flame.     Finally,  mount  in  Canada  balsam. 

The  microscopic  examinations  (x  800  to  1000)  will  show 
an  occasional  leucocyte  and  the  anthrax  bacteria.  There  will 
appear  no  other  visible  formed  elements.  The  nuclei  of  the 
corpuscles  generally  exhibit  a  greenish-blue  tint,  the  anthrax 
rods  are  stained  blue.  The  intensity  of  the  stain  depends  upon 
the  length  of  time  after  death  before  the  films  were  made. 
Usually  the  segment  character  of  all  but  the  shortest  rods  will 
be  apparent.  If  they  are  deeply  stained  this  is  not  very  dis- 
tinct. The  peculiarity  in  the  reaction  lies  in  the  color  of  the 
amorphous  material  which  is  present  between  and  around  the  bac- 
teria. This  material  presents  itself  under  the  form  of  coarse 
or  fine  granules  of  a  violet  or  reddish-purple  color,  which  is  in 
sharp  contrast  to  the  tint  of  the  bacteria  or  cell  nuclei,  espec- 


PKOTKCTIVE    INOCULATION  I47 

ially  with  brilliant  lamp  or  gas  light.  These  violet  granules 
differ  a  good  deal  in  form  and  size  ;  sometimes  they  are  very 
minute,  and  at  others  coarsely  granular.  When  the  bacteria 
are  arranged  in  clumps  the  violet  material  is  often  in  greatest 
amount  about  them.  Free-lying  anthrax  rods  will  be  sur- 
rounded by  a  thick  envelope  of  the  same  substance.  M' Fad- 
yean  states  that  he  has  never  found  this  reaction  in  animals 
dead  from  other  diseases.  The  peculiar  coloring,  he  states, 
in  some  cases  may  be  observed  without  the  aid  of  the 
microscope. 

cj  125.  Protective  inoculation.  Toussaint  was  the  fir.st 
to  make  use  of  protective  inoculations  in  anthrax.  He  heated 
defibrinated  anthrax  blood  to  a  temperature  of  50  to  55°  C.  for 
from  15  to  20  minutes,  then  injected  it  as  a  protective  agent. 
Pasteur,  however,  was  the  first  to  prove  that  immunity  could 
be  obtained  by  the  use  of  cultures  of  attenuated  bacteria. 
Several  methods  of  attenuating  the  specific  organisms  have 
been  proposed  by  Pasteur,  Toussaint,  Chaveau,  Chamberland, 
Arloing  and  others. 

Pasteur's  method  consists  in  inoculating  the  animal  with 
a  small  quantity  of  culture  which  has  been  grown  at  a  high 
temperature— 42  to  43°  C— for  several  days.  This  deprives 
the  bacteria  of  their  virulence.  To  strengthen  the  resistance, 
the  animals  are  again  inoculated  with  a  stronger  virus.  After 
the  two  inoculations,  they  are  said  to  be  protected  against  the 
most  virulent  anthrax  ;  but  the  immunity  is  of  short  duration. 
Chamberland  reported  in  1894  that  a  total  of  1,988,677  animals 
had  been  treated  by  this  method  in  France,  and  that  the  loss 
from  anthrax  had  diminished  from  10  per  cent  in  sheep  and  5 
per  cent  in  cattle  to  less  than  i  per  cent.  Cope,  in  his  report 
to  the  English  Board  of  Agriculture,  regards  the  conclusions 
of  Chamberland  as  somewhat  fallacious,  because  in  order  to 
prove  that  the  animals  inoculated  received  immunity,  it  should 
be  shown  that  they  were  subsequently  exposed  to  the  ri.sks  of 
natural  infection.  The  excellent  work  which  has  been  done 
bv   Neal  and  Chester,   at  the  Delaware    College    Experiment 


148  ANTHRAX 

Station,  has  shown  the  possible  efficiency  of  this  method.  Of 
the  331  cows  which  they  vaccinated  against  anthrax,  two  died 
of  the  disease,  giving  a  death  rate  of  less  than  i  per  cent  and 
this  in  a  territory  so  saturated  with  the  virus  that  it  was  prac- 
tically impossible  to  keep  cattle  at  all  before  its  use. 

A  more  critical  study  of  the  reports  on  the  use  of  this 
vaccine  shows  that  while  success  can  not  be  denied,  failures 
must  be  admitted.  It  is  reported  both  in  England  and  Ger- 
many that  the  Pasteur  vaccine  has  not  been  a  marked  success. 
In  England,  Klein,  who  tested  the  vaccine  used  in  that  coun- 
try, found  that  if  the  animals  did  not  die  from  the  effect  of  the 
vaccine,  they  did  when  exposed  to  the  disease.  The  German 
veterinarians  and  agriculturalists  agree  that  the  first  vaccine 
is  mild  and  harmless,  but  that  the  second  vaccine,  even  in  the 
hands  of  experts,  is  dangerous  and  often  fatal.  In  the  state 
of  Illinois  a  number  of  cattle  died  of  anthrax  immediately 
after  receiving  the  second  vaccine,  and  in  Manitoba  a  large 
number  (about  500)  of  sheep  died  after  the  second  vaccination 
(Higgins).  In  these  cases  the  vaccine  used  was  not  suffi- 
ciently attenuated.  In  a  recent  outbreak  in  the  state  of  New 
York  the  animals  that  were  vaccinated,  but  not  carefully 
isolated  from  the  infected  pastures,  continued  to  die  of  the 
disease  after  the  second  vaccination.  This  was  due  to  the 
excessive  attenuation  of  the  vaccine.  In  the  summer  of  1907 
a  large  number  of  cattle  in  an  infected  territory  were  vaccin- 
ated with  very  good  results.  On  a  few  farms,  all  of  the  unvac- 
cinated  cattle  died  of  anthrax,  while  the  vaccinated  ones 
remained  well.  It  is  reported  to  have  been  demonstrated  by 
experiment  that  the  virulence  of  the  attenuated  virus  can  be 
easily  restored.  Again,  it  has  been  shown  by  the  investiga- 
tions of  Chester  and  Neal,  of  the  Delaware  College  Agri- 
cultural Experiment  Station,  that  a  vaccine  which  succeeded 
at  one  time  subsequently  proved  fatal.  The  vital  objection  to 
this  method  is,  that  it  requires  the  use  of  the  living  bacteria, 
which  later  may  become  virulent  and  consequently  cause  a 
subsequent  outbreak.  The  scattering  of  pathogenic  organisms, 
even  in  an  attenuated  condition,  should  be  avoided  if  possible. 


THE    SIMULTANEOUS    METHOD  I49 

It  must  be  admitted,  however,  that  Pasteur's  method  has  done 
much  good  and  helped  to  rob  anthrax  of  much  of  its  former 
terror,  especially  for  the  farmers  of  Europe.  In  America  the 
spread  of  anthrax  has  been  checked  in  many  districts  by  its 
use.  Dairy mple  has  pointed  out  its  success  in  the  lower  Miss- 
issippi valley.  Notwithstanding,  it  is  highly  probable  that 
the  spreading  of  a  knowledge  of  the  specific  cause  of  this 
disease  with  that  of  the  proper  disposition  of  dead  animals  has 
also  exerted  much  influence  for  good  in  checking  its  ravages. 
In  Germany  and  England  the  stamping-out  system  is  con- 
sidered superior  to  vaccination.  According  to  Crookshank, 
in  England  it  is  regarded  as  the  only  reliable  means  of  sup- 
pressing the  disease.  To  this  end  rigid  laws  have  been  enac- 
ted. In  this  country  as  rigid  measures  as  possible  for  its 
eradication  seem  infinitely  better  than  the  general  adoption  of 
methods  for  establishing  a  tolerance  for  its  existence. 

vj  126.  The  simultaneous  method.  This  method 
which  consists  in  the  injection  of  anthrax  antitoxin  or  serum 
together  with  a  small  quantity  of  virulent  anthrax  bacteria, 
has  proven  to  be  very  satisfactory.  It  has  the  advantage  of 
being  administered  at  one  time.  This  method  of  protection 
against  anthrax  seems  to  have  been  first  proposed  by  Sobern- 
heim  in  1899.  Since  that  time  Sclavo  in  Italy  and  others 
have  published  on  the  method.  Sobernheim  reports  excellent 
results  by  the  use  of  this  method  in  immunizing  cattle  against 
anthrax  in  South  America.  The  serum  is  now  produced  in 
large  quantities  in  Germany.  In  this  country,  it  is  just  begin- 
ning to  receive  attention. 

§  127.  Prevention.  In  all  cases  the  well  animals  should 
be  removed  from  the  barns  or  yards  containing  the  sick  ones 
and  from  pasture  lands  on  which  the  sick  became  infected. 
The^emperature  of  healthy  and  uninfected  animals  should  be 
taken  morning  and  evening  for  from  one  to  two  weeks  after 
they  are  removed  and  all  of  those  showing  an  elevation-  of 
temperature  should  be  isolated.  By  careful  isolation  and  safe 
disposition  of  the  dead  animals  the  spread  of  the  disease  can  be 


150  ANTHRAX 

checked.  Animals  do  not,  as  a  rule,  spread  the  virus  when  the 
first  symptom  (rise  of  temperature)  can  be  detected.  All 
infected  stables  and  yards  should  be  thoroughly  disinfected. 

Tlie  disposition  of  dead  animals  in  an  outbreak  of  anthrax 
is  a  matter  of  much  importance.  In  all  cases  they  should  be 
burned  if  possible,  if  not,  they  should  be  buried  deeply  and 
covered  with  quick  lime  before  the  dirt  is  replaced.  The 
ground  over  the  place  where  they  are  buried  should  be  fenced 
in  to  prevent  other  animals  from  grazing  over  it,  and  the  sur- 
face should  be  burned  annually  for  some  years  to  destroy 
spores  should  they  be  brought  to  the  surface. 

REFKRENCKS. 

1.  Burnett.  On  the  control  of  an  outbreak  of  anthrax.  Ant. 
Vet.  Revieiv.     1908. 

2.  Chester.  Anthrax,  bacteriological  work.  Report  Del.  Agr. 
E.vpt.  Station,  1895,  p.  64. 

3.  Chester.  Protective  inoculation  against  anthrax.  Proceed- 
ings of  the  Society  for  the  ProDiotion  of  Agricultural  Science,  iS96,p.  52. 

4.  Dalrympi^e.  Anthrax  and  protective  inoculation  in  Louisiana. 
Proceedings  of  the  A))i.  Vet.  Med.  Assn.,  1901,  p.  147. 

5.  Davaine.  Recherches  sur  les  infusoires  du  sang  dans  la  mal- 
adies connue  sous  le  nom  de  sang  de  rate.  Compt.  Rend,  de  V  Acad, 
des  Sc.  1863,  1864,  1865. 

6.  KoCH.  Die  Aetiologie  der  Milzbrand-Krankheit  begriindet  auf 
die  Entwickelungsgeschichte  des  Bacillus  Anthracis.  Colin' s  Beitr. 
ziir  Biol,  der  Pflanzen,  Bd.  II  (1876),  vS.  277. 

7.  M'Fadyean.  Anthrax,  four.  Couipar.  Bath,  and  Ther..  \'ol. 
XI  (1898).  p.  51. 

8.  M'Fadvean.  a  peculiar  staining  reaction  of  the  blood  of  ani- 
mals dead  of  anthrax,  four,  of  Couipar.  Path,  and  Ther.,  \o\.  XVI 
(1903),  p.  35. 

9.  M'Fadvean.  Extraneous  sources  of  infection  in  outbreaks  of 
anthrax,    four.  Conipar.  Path,  and  Ther.,  Vol.  XVI,  p.  346. 

10.  Moore.  Report  of  an  outbreak  of  anthrax.  Annual  Report, 
Comtnissioner  of  Agriculture  of  the  State  of  New  Yorl^.     1897. 

11.  Pasteur,  Chamberland  et  Roux.  De  Tattenuation  des 
virus et  de  leur  retour  a  la  virulence.  Coinp.  Rend,  de  P  Acad,  des  Sc, 
Vol.  XCII  (1881),  p.  427. 


GLANDERS  15I 

12.  PasTKIR.      La  vaccin  du  charbon.      Ibid.     p.  6b6. 

13.  RiSSELL.  Outbreak  of  anthrax  fever  traceable  to  tannery 
refuse.      The  ijth  annual  report  of  the  Wis.  Agric.  Exp.  Station,  1889. 

14.  SoBERNHEiM.  Ueber  das  Milzbrandserum  und  seine  praktische 
Anwendung.  Deut.  med.  IVochenschr.,  1904.  No.  26  u.  27.  (First 
publication.     Zeit.fi'ir  Hygiene,  1899,  Bd.  31). 


GLANDERS 
Sytumyms.      Malleus;  farcy;   morve  \  Rotzkrankheit. 

i^  128.  Characterization.  Glanders  is  one  of  the  most 
important  diseases  of  horses,  asses  and  mules  and  when  trans- 
mitted to  man,  one  of  the  most  fatal  diseases  of  the  human 
species.  It  runs  an  acute  or  chronic  course,  attacking  the  lym- 
phatic system  more  especially  in  the  upper  air  passages,  lungs 
or  skin.  The  disease  is  characterized  by  a  strong  tendency  to 
the  formation  of  small  neoplasms  or  nodules  which  are  likely 
to  degenerate  into  ulcers  from  which  exudes  a  peculiar  .sticky 
di.scharge.  In  the  very  acute  cases  a  considerable  rise  of  tem- 
perature and  general  debility  may  accompany  the  formation  of 
the  lesions.      Glanders  of  the  skin  is  known  as  farcy. 

By  direct  inoculation  several  species  of  animals  may  be 
infected.  Thus  the  disease  has  been  reported  in  goats,  rab- 
bits, sheep,  guinea  pigs,  field  mice,  and  several  of  the  wild 
animals,  especially  those  of  the  cat  tribe.  Swine  and  pigeons 
are  very  slightly  susceptible.  Cattle,  white  mice,  rats  and 
domestic  fowls  seem  to  be  immune. 

^  129.  History.  The  theory  of  the  contagiousness  of 
glanders  was  much  doubted  at  the  beginning  of  this  century. 
The  view  taken  by  the  veterinarians  at  the  Alfort  Veterinary 
College  was  that  glanders  might  arise  spontaneously  from  an 
attack  of  strangles.  This  view  was  far  more  widely  accepted 
than  the  theory  of  its  contagiousness,  which  was  stoutly  sup- 
ported by  the  authorities  at  the  Veterinary  College  of  Lyons. 
It  was  not  until  Rayer  (1837)  had  demonstrated  the  trans- 
missibility    of  glanders   to    man,    and    Chauveau  (1868;)   had 


152  GLANDERS 

shown  that  the  virus  was  contained  chiefly  in  the  firm  compo- 
nent parts  of  the  infective  material,  that  the  fact  of  the  infec- 
tious nature  of  the  disease  was  accepted. 

The  theory  of  the  spontaneous  origin  of  glanders  was 
widely  accepted  in  Germany.  Sixty  years  ago  it  was  believed 
that  glanders  could  be  produced  by  the  injection  of  pus,  and 
that  strangles  could  develop  into  glanders.  Glanders  was 
looked  upon  as  a  tubercular  disease,  scrofula,  pyemia,  diph- 
theritis,  general  dyscrasia  and  cachexia  respectively.  Vir- 
chow  was  the  first  to  declare  that  the  nodules  of  glanders  were 
independent,  anatomical  formations,  which  he  placed  under 
the  heading  of  granulation  tumors.  Gerlach  was  the  strong 
advocate  for  the  exclusively  infectious  origin  of  the  disease. 
Leisering  appears  to  have  been  the  first  to  give  an  accurate 
description  of  the  lesions. 

The  first  biological  researches  into  its  nature  were  made 
in  1868  by  Zurn  and  Hallier,  who  found  a  fungus  which  they 
believed  to  be  its  cause.  In  1882,  Loeffler  and  Schiitz  suc- 
ceeded in  finding  the  bacterium  of  glanders,  in  cultivating  it, 
and  in  transmitting  the  disease  to  other  animals  by  inoculating 
them  with  pure  cultures  of  the  organism.  Their  researches 
furnished  the  positive  proof  that  glanders  is  a  specific,  infec- 
tious disease,  produced  exclusively  by  Bacterium  mallei. 

§  130.  Geographical  distribution.  Glanders  exists  in 
the  greater  part  of  the  civihzed  world.  It  is  more  common  in 
the  temperate  zones,  where  traffic  in  horses  is  active.  In  the 
United  States  it  was  largely  confined  to  the  Northern  States 
before  1861,  but  it  spread  over  the  South  in  connection  with 
the  civil  war.  It  is  said  to  have  entered  Mexico  with  the 
American  cavalry  in  1847.  Similarly,  Portugal  is  said  to  have 
been  exempt  until  the  invasion  by  Napoleon  in  1797.  Central 
Hindoostan  was  said  to  be  free  from  it  until  the  war  with 
Afghanistan  in  1878.  In  all  these  cases,  the  movements  of 
cavalry,  artillery  and  of  commissary  trains  were  responsible 
for  the  introduction  of  the  disease  into  new  territory.  In  our 
own  case  the  sale  of  horses  and  mules  at  the  close  of  the   civil 


ETIOLOGY  153 

war  produced  a  very  general    diffusion    of    this   disease,    from 
which  the  country  is  still  suiTering. 

Insular  places,  especially  if  far  from  the  main  land  and 
free  from  importation  of  horses,  usually  escape.  Thus  glanders 
is  very  rare  in  Iceland  and  in  the  Faroe  islands.  In  Australia, 
Tasmania  and  New  Zealand  it  is  reported  to  be  unknown. 

^  131.  Etiology.  Baderiiun  mallei,  the  specific  cause 
of  glanders,  was  discovered  and  isolated  in  pure  culture  almost 
at  the  same  time  (1882)  by  Loeffier.  Schiitz,  Israel,  Bouchard, 
Charrin.  Weichselbaum,  Kauzfeld  and  Kitt.  It  is  found  in 
the  recent  nodules,  in  the  discharge  from  the  nostrils,  pus  from 
the  specific  ulcers,  and  occasionally  in  the  blood  of  animals 
affected  with  glanders. 

Morphologically  it  is  a  small  organism  with  rounded  or 
pointed  ends.  It  varies  in  breadth  from  o.25/<  to  o.4/<  and 
from  i.5/<  to  3//  in  length.  It  is  usually  single  but  pairs  and 
long  filaments,  especially  on  potato  cultures,  are  not  rare.  It 
frequently  breaks  into  short,  almost  coccus-like  elements. 
Galli-Valerio  found  great  variations  in  its  morphology  when 
grown  under  certain  different  conditions.  Branching  forms 
were  numerous. 

It  stains  with  some  difficulty.  Of  the  aniline  colors,  the 
best  results  are  obtained  with  the  aqueous  solutions,  when  they 
are  made  feebly  alkaline.  It  is  decolorized  by  Gram's  method. 
It  grows  well,  but  slowly,  at  the  body  temperature  on 
glycerin  agar,  in  acid-glycerin  bouillon,  on  blood-serum  and 
on  potato. 

Of  the  test  animals,  guinea  pigs  and  field  mice  are  the 
most  .susceptible.  In  guinea  pigs,  subcutaneous  injections  are 
followed  in  four  or  five  days  by  swelling  at  the  point  of  inocu- 
lation and  sloughing  of  the  skin,  which  are  followed  by  the 
formation  of  a  chronic,  purulent  ulcer.  The  lymphatic  glands 
become  inflamed  and  symptoms  of  general  infection  develop 
in  from  two  to  four  weeks  ;  the  glands  suppurate  and  in  males 
the  testicles  are  involved.  A  purulent  inflammation  of  the 
joints  may  occur.     The  formation  of  the   specific  ulcers  upon 


154  GLANDERS 

the  nasal  mucous  membrane,  which  forms  one  of  the  charac- 
teristics of  the  disease  in  the  horse,  rareh'  occurs  in  the  guinea 
pig  as  a  result  of  inoculation.  The  disease  is  often  prolonged 
for  several  weeks  or  months.  Guinea  pigs  succumb  usually 
in  from  eight  to  ten  days  when  injected  into  the  peritoneal 
cavity  with  a  virulent  culture.  In  males,  the  testicles  are 
invariably  affected. 

The  period  of  i7iciibation  is  not  generally  known.  It  evi- 
dently varies  from  a  few  to  many  days. 

§  132.  Symptoms.  Two  forms  of  glanders  have  been 
recognized,  namely,  acute  and  chronic. 

Acute glandtrs.  Acute  glanders  is  common  in  the  ass  and 
mule,  but  infrequent  in  the  horse.  After  a  short  period  of  in- 
cubation the  animal  has  a  chill,  elevation  of  temperature,  a 
profuse  muco-purulent,  sticky  discharge,  sometimes  mixed, 
with  blood,  from  the  nose.  Particles  of  food  arrested  in  the 
pharynx  occasionally  appear  in  the  nasal  discharge.  If  uni- 
lateral the  margin  of  the  nostril  swells,  the  mucosa  is  dark 
red,  infiltrated,  marked  with  pea-like,  yellowish  elevations 
with  red  areolae,  which  in  a  few  days  become  eroded,  thus 
forming  spreading  ulcers.  The  submaxillary  lymphatic 
glands  on  the  affected  side  become  enlarged.  There  may, 
however,  be  a  uniform  swelling  of  the  intermaxillary  space. 
The  course  is  rapid  and  death  ensues  in  from  the  sixth  to  the 
fifteenth  da}'.     The  acute  form  rarelj'  if  ever  becomes  chronic. 

Chronic  glanders.  In  the  horse,  this  form  of  the  disease 
may  begin  with  a  chill  but  usually  the  onset  is  very  insidious. 
There  may  be  a  muco-purulent,  sticky  discharge,  sometimes 
streaked  with  blood,  from  one  or  both  nostrils.  There  may 
be  intermittent  or  continued  lameness,  arthritis,  edema  of  a 
limb,  swelling  of  a  testicle,  cough,  or  epistaxis.  There  is 
usuall}'  a  nodular  but  comparatively  painless  swelling  of  the 
submaxillary  lymph  gland  on  the  affected  side.  On  palpation 
the  swelling  imparts  a  sensation  suggestive  of  a  number  of 
peas.  They  are  adherent  to  the  adjacent  structures.  The 
nasal    mucosa    is    congested,    of    a    dark    reddish     color    and 


MORBID    ANATOMY  155 

sprinkled  with  superficial  or  deep  ulcers  either  clean  or 
covered  with  crusts. 

Rarely  the  submaxillary  glands  only  are  apparently  dis- 
eased. In  other  cases,  there  is  only  a  cough,  the  latent  lesions 
being  confined  to  the  lungs.  In  still  other  cases,  the  lesions 
are  restricted  to  one  or  both  testicles,  the  spleen,  or  some  other 
internal  organ.  Objective  symptoms  may  or  may  not  be 
present.      Chronic  glanders  may  terminate  in   the  acute  form. 

In  chronic,  cutaneous  glanders,  with  or  without  edema  of 
the  limbs,  there  may  be  one  or  many  nodules  on  the  fetlock, 
or  elsewhere  on  the  line  of  the  lymphatic  vessels,  with  indura- 
tion of  the  lymphatics  extending  from  it.  The  nodules  may 
be  suppurating  and  discharging,  or  they  may  be  closed. 

?;  133.  Morbid  anatomy.  In  chronic  glanders  the  most 
frequent  locations  of  the  lesions  are  on  the  respiratory  mucous 
membrane,  in  the  lungs,  lymph  glands  and  skin.  M'Fadyean 
states  that  he  has  never  seen  a  case  of  glanders  in  which  the 
lungs  were  not  affected  if  any  lesions  were  found.  Other 
organs  are  more  rarely  invaded.  The  mucous  membrane  of 
the  upper  respiratory  passages  is  the  usual  seat  of  the  lesions. 
Glanders  occurs  in  two  forms,  (i)  as  circumscribed  nodules 
with  the  formation  of  ulcers  and  cicatrices  ;  and  (2)  as  diffuse 
or  infiltrated  lesions. 

In  nodulaf  glanders,  which  is  the  common  form,  the 
lesions  are  most  frequently  situated  on  the  upper  portion  of 
the  nasal  septum  and  in  the  cavities  of  the  turbinated  bones. 
The  affection  begins  with  the  appearance  of  nodules  varying 
in  size  from  a  grain  of  sand  to  a  millet  seed.  They  are  more 
or  less  translucent,  of  a  roundish  or  oval  shape,  and  of  a  dirty 
gray  or  grayish-red  color.  The  nodules,  which  may  attain  to 
the  maximum  size  of  a  pea,  project  somewhat  above  the  sur- 
face of  the  mucous  membrane.  They  are  surrounded  by  a 
reddish  ring.  Some  of  them  are  isolated  and  others  are 
arranged  in  groups.  Microscopically  they  consist  of  a  large 
number  of  lymphoid  cells,  which  disintegrate  in  the  centre  of 
the  nodule.     In  consequence  of  the  central  fatty  and  purulent 


156 


GLANDERS 


degeneration,    the    nodules    become   yellowish    in    color,    dis- 
charge and  form  ulcers.     These  ulcers  are  sometimes  super- 
ficial, sometimes  deep, 
lenticular   or    crateri- 
form,   surrounded    by 
a      hard,       indurated 
edge,    and  frequently 
becoming     confluent, 
with    irregularly    ser- 
rated     and       eroded 
edges.         They      are 
sometimes        covered 
with  a  brownish  crust. 
The    ulcers    may    in- 
crease   in    area   or   in 
depth  and  may    even 
involve    the    underly- 
ing cartilage  or  bone, 
causing  perforation  of 
the  septum  nasi,  and 
distensions      of      the 
maxillary  or  exostoses 
on       the      turbinated 
bones.      The  shallow 
lenticular  ulcers  may 
heal    without  leaving 
any   visible  .changes  ; 
but   the  deeper  ones, 
after      granulating, 
leave    a     radiating, 
star-shaped      cicatrix 
which  is  either  smooth 
or  horny,  and  which, 
according  to  the  shape 
of  the  ulcer,    may  be 
of  an  irregular  or  oblong  form.     The  nasal  septum  is  frequently 
covered  with  these  scars.     The  ulcers  and  cicatrices  are  some- 


FiG.  24.  Nasa/  septum  atid  portion  of 
turbinated  bone  shouiing  glanders  ulcers 
'with  tcvo perforations  (  Williams). 


MORBID    ANATOMY 


157 


times  found  in  the  maxillary  and  frontal  sinuses,  in  the  gut- 
tural pouches  and  in  the  eustachian  tubes.  They  may  also 
occur  in    the    larynx,    especially    in    the    region  of  the  vocal 


Fig.  25.  Photograph  of  a  portion  of  a  tiasal  septum  shoivitig  ulcers  in 
advanced  glanders:  {a)  perforations  of  septum,  {h)  conjluent  ulcers  and 
necrotic  tissue. 


158 


GLANDERS 


chords.  In  the  trachea  and  even  in  the  bronchi,  particularly 
on  the  anterior  surface,  numer- 
ous long,  oval  ulcers  or  long, 
pointed,  serrated  scars  are  fre- 
quently found.  In  addition  to 
the  ulcers,  a  catarrhal  inflamma- 
tion of  the  mucous  membrane  is 
very  apt  to  be  present. 

Diffuse  glanders  manifests  it- 
self as  a  diffuse  catarrh  of  the 
mucous  membrane  of  the  nasal 
and  neighboring  cavities,  with 
superficial  ulceration,  thrombosis 
of  the  veins,  inflammatory  in- 
filtration of  the  submucosa.  con- 
siderable thickening  of  the  mu- 
cous membrane  and  the  forma- 
tion of  a  peculiar,  radiating  cica- 
trix. 

Both  the  nodular  and  infil- 
trated forms  are  found  in  the 
lungs. 

In  the  nodular  form,  the  lungs 
contain  nodules-'^  varying  in  size 
from  a  millet  seed  to  a  pea. 
They   are   gray    by    transmitted 


*Nocard  showed  that  when  glan- 
dered  horses  are  treated  with  mallein, 
a  certain  proportion  of  them  recover, 
in  which  case  nodules  that  are  pres- 
ent in  the  lungs  cease  to  contain 
living  bacteria,  a  fact  he  has  fully 
proved  by  inoculation.  On  post- 
mortem examination  the  nodules 
may  be  readily  felt  by  passing  the 
hand  with  firm  pressure  over  the  sur- 
face of  the  lung,  which,  when  badly  diseased,  will  feel  like  a  bag  full 
of  shot  or  peas. 


Fig.  26.  A'asd/  Sifl/nn  froii  a 
slandered  Iwrse  slwiving  two 
large  scars  and  several  smal- 
ler recent  healing  ulcers  and 
scars   {Williatns). 


MORBID    ANATOMY 


159 


light,  glassy  and  pearl  gray  by  reflected  light,  and  are  sur- 
rounded by  a  congested  or  a  hemorrhagic  ring.  The  center  of 
the  nodules  shows  a  pale  yellow  point  in  consequence  of  casea- 
tion and  disintegration  of  the  innermost  cells.  These  nodules 
are  of  different  sizes,  of  varying  numbers,  and  of  different 
ages.  The  formation  of  a  capsule  by  a  connective  tissue  mem- 
brane is  induced  by  a  reactive  inflammation  in  the  tissue  sur- 
rounding the  nodule.     The  nodules  may    be   of   an    embolic 


Fig.  27.     Drazving  of  a  horse's  lung  containing  glanders  nodules  (<?). 
They  appear  on  both   the  pleural  and  cut  surfaces. 

origin  situated  principally  in  the  periphery  of  the  lung,  their 
structure  being  the  same  as  that  of  the  nodules  in  the  nasal 
mucosa.  Sometimes  the  lung  nodules  represent  lobular  pneu- 
monic foci,  in  which  the  alveoli  are  filled  with  red  and  white 
blood  corpuscles  and  with  desquamated  epithelium  of  the 
lungs.  Central  disintegration  occurs  very  early.  These  areas 
are  surrounded  bv  a  membrane  resulting  from  a  reactive  in- 
flammation which  manifests  itself  and  out  of  which  a  connec- 
tive tissue  capsule  develops  later  on.  There  are  two  theories 
concerning  the  structure  of  the  early  nodules.  One  is,  that 
the  first  cells  are  epithelial  in  nature,  thus  closely  resembling 


l6o  GLANDERS 

a  tubercle.  The  other  is  that  the  first  stage  of  the  nodules 
consists  of  air  cells  filled  with  leucocytes. 

M'Fadyean  has  called  attention  to  the  structure  of  the 
lung  nodules,  in  which  he  finds  a  central  part  composed  of 
leucocytes  that  have  filled  the  air  spaces,  the  walls  of  which 
have  disappeared  as  if  by  liquefaction.  This  is  surrounded  by 
a  zone  of  epithelioid  cells.  A  third  zone  surrounds  this,  in 
which  the  walls  of  the  air  vesicles  are  recognizable.  The 
walls  are  thickened.  The  fourth  zone  is  composed  of  air  ves- 
icles filled  with  a  fibrinous  exudate,  which  entangles  a  few 
leucocytes.  Frequently  the  exudate  is  free  from  red  blood 
corpuscles,  but  at  times  it  contains  much  blood.  In  older 
nodules  the  third  and  outermost  zone  is  composed  of  cirrhotic 
lung  tissue,  in  which  can  be  distinguished  the  remains  of  the 
air  cells.  This  zone  passes  gradually  into  the  normal  tissue. 
In  the  last  stage  the  central  area  shrinks  and  becomes  calcified, 
while  the  other  zones  become  converted  into  a  distinct  fibrous 
capsule.  Other  observers  have  not  reported  the  calcification. 
It  has  not  occurred  in  the  writer's  observation.  The  cell 
necrosis  in  glanders  has  been  designated  by  Unna  as  chroma- 
tolasis  which  consists  in  the  disintegration  of  the  nucleus  before 
the  destruction  of  the  cell  body  and  the  retention  of  the  stain- 
ing property  of  the  broken,  nuclear  chromatin.  This  gives 
the  dark  color  in  the  central  part  of  a  stained  nodule. 

Besides  these  nodules,  there  are  often  chronic  bronchitis, 
peribronchitis,  parabronchitis,  atelectasis,  inflammation  of  the 
tissue  of  the  lung  and  less  frequently  circumscribed  or  exuda- 
tive pleuritis. 

Infiltrated  glanders  of  the  lungs  form  tumors  from  the 
size  of  a  walnut  to  that  of  a  child's  head,  consisting  of  a  diffuse 
glanderous  infiltration  of  the  alveoli  and  of  the  interstitial 
connective  tissues.  Frequently  on  section  the  infiltrated  parts 
of  the  lungs  resemble  very  closely  a  soft  sarcoma.  They  are 
of  a  dirty  white  color,  of  a  gelatinous,  juicy  consistency  and 
irregular  in  shape.  They  may  either  become  indurated  so  as 
to  form  hard,  connective  tissue-like  new  growths  (fibroma-like 
tumors  of  glanders,  according  to  Gerlach),  or  they  may  become 


MORBID    ANATOMY 


l6l 


gangrenous.     In   nodular  and  in  infiltrated    glanders   of  the 

lungs,  the  bronchial  glands   and    frequently    the    mediastinal 

glands  become   enlarged,    indurated   and   studded   with   small 

foci  of  cell  infiltration. 

In   glanders  of  the   skin   (farcy)  the  nodules  are  found  in 

the  papillary  layer,  in  the  cutis  and  in  the  subcutaneous  and 

superficial  intermuscular 

tissue.       The  cutaneous 

nodules     vary     in     size 

from  a  hemp  seed  up   to 

a  pea.      They  suppurate 

rapidly   and   form  small 

ulcers.     The  nodules  in 

the  subcutis  are  inflam- 
matory (metastatic)  tu- 
mors from  the  size  of  a 
pea  to  that  of  a  hen's 
egg.  They  change  into 
large  abscesses  and  dis- 
charge externally.  In 
the  region  of  the  nodules 
the  lymphatic  vessels 
are  inflamed,  swollen, 
and  frequently  resemble 
a  rosary  or  knotted  cord. 
Ulcers  often  develop 
from  these  secondary 
nodes.  The  neighbor- 
ing lymph  glands  are  at 
first  swollen  and  soft, 
but  later  they  become  indurated  by  the  growth  of  connective 
tissue  and  studded  with  dirty  white  nodules  about  as  large  as 
a  pin  head,  or  with  yellow  foci  of  caseation.  The  capsule 
around  the  lymph  glands  becomes  infiltrated  with  small  cells 
and  subsequently  thickened.  In  rare  cases  secondary  chronic 
farcy  occurs.  It  is  marked  by  a  large,  diff"use  new  growth  of 
connective  tissue  with  nodular  thickening 


tiG.    2^.        J>l'(lHm    (>/    (I    i;  Ul/ntt:  I  J    :n    liiiU" 

in  the  lung  of  a  horse:  (a)  necrotic  center, 
{c)  zone  of  giant  cells,  (d)  capsule  stir- 
ro II  nding  the  nodii le  ( Sch  i'ltz ) . 


of  the  skin.     This 


l62  GLANDERS 

condition  is  termed  glanderous  elephantiasis  or  pachyderma. 
It  chieflv  affects  the  limbs  and  head. 


r' 

^_i 

r  ^i4VL 

l5 

^^^Hi^^  'V            ^^^^^^^^^^1 

K^-^^^^^H 

1 

Fig.     29.      Photogyaph   sho-wing   cutaneous  glanders  or  farcy   buds. 
{Photograph  by  Kelly). 


GLANDERS    IN    MAN 


163 


Of  the  abdominal  organs,  the  spleen  is  most  frequently 
attacked.  It  then  contains  embolic  uodules,  which  vary  iu 
size  and  either  suppurate  or  become  calcareous.  vSimilar 
nodules  occur,  though  not  so  often,  in  the  liver,  kidneys, 
testicles,  brain,  muscles,  heart  and  bones.  In  the  bones,  the 
lesions  consist  of  a  cellular  infiltration  of  the  medulla  and 
purulent  breaking  down  of  the  osseous  tissue.  Ulcers  are 
very  rare  on  the  mucous  membranes  of  the  eyes,  stomach  and 
vagina.  The  blood  shows  signs  of  shght  leucocytosis.  The 
specific  bacteria  are  found  in  the  blood  only  in  cases  of  acute 
general  infection. 

The  anatomical  changes  in  acute  glanders  consist  chiefly 
in  a  disintegration  of  the  respiratory  mucous  membrane,  in  a 
serous  infiltration  of  the  submucosa,  subcutis,  and  inter- 
muscular tissue,  with  inflammation  and  suppuration  of  the 
lymph  vessels  and  lymph  glands.  There  are  also  metastatic 
formations  in  the  skin  and  lungs.  The  nasal  mucous  mem- 
branes are  covered  with  rapidly  spreading  ulcers  with  consid- 
erable infiltration  into  the  submucosa.  The  mucous  membrane 
of  the  larynx  and  pharynx  may  be  swollen  and  covered  with 
ulcers.  The  lungs  are  studded  with  purulent  metastatic  foci 
or  fresh  nodules.  The  skin  is  excessively  swollen  and  covered 
with  glanderous  nodes.  Sometimes  diffuse  gangrene  of  the 
skin  occurs. 

ji  134.  Glanders  in  man.  The  symptoms  of  glanders 
in  man  are  of  much  importance  to  the  veterinarian.  Although 
the  susceptibility  to  the  disease  is  usually  not  very  great,  cases 
of  human  glanders  unfortunately  occur,  especially  among 
veterinary  surgeons  and  those  having  the  care  of  horses. 
Human  glanders  is  reported  to  be  (juite  common  in  Russia. 
The  parts  usually  first  affected  are  the  hands,  nasal  mucous 
membrane,  lips  and  conjunctiva.  After  a  period  of  incubation 
of  from  three  to  five  days  the  infected  part  becomes  swollen 
and  painful,  with  subsequent  inflammation  of  the  lymph  ves- 
sels and  swelling  of  the  glands.  Fever  is  often  the  first 
symptom,  and  it  is  nearlj'    always    followed    by    a    nasal    dis- 


164  GLANDERS 

charge,  ulcers  on  the  nasal  mucous  membrane,  pustules  and 
abscesses  in  the  skin,  ulcers  in  the  oral  cavity,  larynx,  and 
conjunctiva,  articular  swellings,  and  grave  general  distur- 
bances. Sometimes  there  is  intense  gastrointestinal  trouble. 
Nodules  occur  in  the  lungs  in  some  cases.  As  a  rule,  death 
takes  place  in  from  two  to  four  weeks,  and  occasionally  in  a 
few  days.  In  other  instances,  the  disease  becomes  chronic, 
lasting  for  months  or  years.  Bad.  mallei  has  been  found  in 
the  blood  in  cases  of  acute  glanders.  The  positive  diagnosis 
depends  on  the  possibility  of  infection  having  taken  place,  on 
inoculation  in  guinea  pigs,  or  the  proof  of  the  presence  oi  Bad. 
mallei.  Treatment  is  usually  of  no  avail.  The  only  hopeful 
cases  are  those  that  are  purely  local  in  their  manifestation. 
A  few  of  these  are  reported  to  have  been  cured  by  applying 
deep  cauterization. 

§  135.  Differential  diagnosis.  Glanders  is  to  be  differ- 
entiated from  a  variety  of  nasal  and  lymphatic  disorders  more 
or  less  common  in  the  horse  kino.  Before  the  discovery  of 
the  specific  bacterium  of  glanders  or  of  mallein,  it  was  neces- 
sary to  determine  as  closely  as  possible  the  differential  anato- 
mical characters  between  glanders  and  those  of  other  affec- 
tions, such  as  chronic  nasal  catarrh,  strangles,  lymphangitis, 
follicular  ulceration  of  the  nasal  mucosa,  cancer,  sarcoma, 
actinomycosis,  melanosis  and  the  like.  Strong  has  described 
a  disease  in  the  Philippine  Islands,  which  first  appears  in 
nodules,  that  resemble  those  of  glanders  very  closely.  It  is 
caused  by  a  blastomyces.  It  occasionally  attacks  cattle  as 
well  as  horses.  The  disease  most  liable  to  be  mistaken  for 
farcy  or  skin  glanders  is  epizootic  lymphangitis  caused  by  a 
yeast-like  fungus  {Saccharomyces  farcimi?ios7is) .  This  disease 
has  recently  been  discovered  by  Pearson  in  Pennsylvania. 

Since  the  discovery  of  practically  positive  means  of  diag- 
nosis, it  does  not  seem  wise  to  speculate  upon  the  chances  of 
a  correct  differential  determination  by  obscure  clinical  evi- 
dences. If  the  diagnosis  of  glanders  can  not  be  made  from  the 
symptoms  and  lesions   in    evidence    three    reliable    diagnostic 


MALLEIN  165 

procedures  are  available.     These  are   animal   inoculation,   the 
use  of  mallein  and  the  agglutination  or  serum  test. 

Animal  inoculation.  Male  guinea  pigs  should  be  used. 
The  material  for  inoculation  usually  consists  of  the  nasal  dis- 
charge from  the  suspected  glandered  horse,  bits  of  scrapings 
from  the  ulcers,  or  pieces  of  other  diseased  tissue.  The 
method  to  be  followed  is  precisely  the  same  as  with  the  sub- 
cutaneous inoculation  of  tuberculous  material.  In  these  cases 
there  is  liable  to  be  a  local  swelling  and  abscess.  The  first 
symptom  of  glanders  noticed  is  usually  orchitis.  The  lym- 
phatic glands  in  the  groin  are  also  enlarged.  After  the 
orchitis  becomes  well  advanced,  the  guinea  pig  may  be  chloro- 
formed and  examined.  Pure  cultures  of  the  specific  organism 
can  be  obtained  in  most  cases  from  the  suppurating  foci  in  the 
testicle.  The  spleen  is  usually  enlarged  and  sprinkled  with 
grayish  nodules.  Other  organs  may  be  involved.  The  diag- 
nosis by  the  inoculation  of  a  male  guinea  pig  is  known  as  the 
Strauss  method. 

Mallein.  Mallein  is  prepared  in  the  same  way  as  tuber- 
culin. It  consists  of  the  glycerinated  bouillon  in  which  the 
glanders  bacteria  have  grown  and  in  which  are  the  products 
resulting  from  their  multiplication.  It  has  a  somewhat  fetid 
odor.  In  applying  the  mallein  test  the  horse  is  injected 
usually  in  the  neck  with  the  required  amount  (0.5  to  2  cc.)  of 
mallein,  the  quantity  depending  upon  the  degree  of  concentra- 
tion. If  a  concentrated  mallein  is  used  it  should  be  diluted 
with  a  I  per  cent  carbolic  acid  solution  to  at  least  2  cc.  The 
reaction  is  as  follows.  In  a  few  hours  there  forms  at  the  place 
of  injection  a  hot,  inflammatory  swelling.  It  is  very  painful 
and  in  case  of  glanders  quite  large.  From  all  sides  of  the 
swelling  there  may  radiate  wavy  lines  consisting  of  swollen 
lymphatics,  hot  and  painful  when  touched,  extending  toward 
the  adjoining  glands.  When  the  mallein  injection  is  made 
aseptically,  this  swelling  never  suppurates,  but  it  increases  in 
size  during  a  period  of  from  24  to  36  hours  and  persists  for 
several  days,  when  it  gradually  diminishes  and  finally  disap- 
pears at  the  end  of  eight  or   ten  days.      With   the   appearance 


1 66  GLANDERS 

of  the  local  swelling  the  patient  becomes  dull  and  dejected, 
the  eyes  have  an  anxions  expression,  the  coat  is  lusterless,  the 
flanks  contracted,  the  respiration  hurried  and  the  appetite  is 
impaired.  Frequent  shudders  are  observed  to  pass  through 
the  muscles  of  the  fore  legs  and  sometimes  the  trunk  is  subject 
to  violent  convulsive  movements.  The  most  active  and 
fractious  horses  become  listless  and  indifferent  to  their  sur- 
roundings. These  general  phenomena  constitute  what  the 
French  call  the  "organic  reaction,"  but  they  are  not  always 
so  clearly  marked.  Differences  in  their  intensity  are  observed 
but  they  are  never  completely  absent. 

The  temperature  reaction  never  fails  to  show  itself.  In 
about  eight  hours  after  the  injection  the  temperature  of  a  glan- 
dered  horse  gradually  rises  1.5°,  2°  or  2.5°  F.,  and  even  more 
above  the  normal.  The  rise  in  temperature  usually  attains  its 
maximum  between  the  tenth  and  twelfth  hour,  occasionally 
not  till  the  fifteenth,  and  more  rarely  not  until  about  the 
eighteenth  hour.  An  important  fact  to  note  is  that  the  reac- 
tion called  forth  in  glandered  horses  by  the  injection  of  mallein 
persists  for  from  24  to  48  hours  and  in  some  cases  the  temper- 
ature remains  above  the  normal  for  even  a  longer  time.  In 
practice  it  is  advisable  to  take  the  temperature  of  the  suspected 
animals  two  or  three  times  before  the  injection  of  the  mallein, 
and  every  two  hours,  beginning  at  the  eighth  and  going  to  the 
twentieth  hour  after  the  injection.  It  is  often  suflBcient  for 
diagnostic  purposes  to  take  the  temperature  but  four  times, 
viz.,  at  9,  12,  15,  and  18  hours  after  the  injection. 

In  healthy  horses  the  injection  of  mallein,  even  in  a  much 
larger  dose,  produces  no  effect  on  the  temperature  or  the  gen- 
eral condition  of  the  animal.  There  is  produced,  however,  at 
the  point  of  injection,  a  small  edematous  swelling,  somewhat 
hot  and  painful  to  the  touch,  but  the  edema  instead  of  increas- 
ing, diminishes  rapidly  and  disappears  in  less  than    24   hours. 

The  reaction  called  forth  by  the  injection  of  mallein  in  a 
glandered  animal  is  quite  specific.  When  it  occurs  one  is 
enabled  to  state  at  once  and  with  certainty  that  glanders  exists, 
although  the  lesions  may  be  quite  minute  or  obscure.     When 


MALLEI  N 


167 


the  reaction  does  not  take  place  it  is  generally  considered  that 
the  animal  tested  is  not  glandered,  although  the  physical 
examination  may  suggest  it.  Notwithstanding  the  specific 
action  of  mallein,    its    administration    can    give    really    useful 


0 

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AM. 
6 

A.M.    , 

A.M. 

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P.M. 
4 

7?M. 
6 

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FIG  30.  Mallein  reaction.  Teviperature  curves  of  six  hordes  for  24 
hours  after  injecting  mallein.  The  horses  7cere  in  one  stable  Jrom 
zvhich  a  well  developed  case  of  glanders  had  been  removed. 


l68  GLANDERS 

indications  according  to  Nocard  "only  when,  and  as  far  as,  we 
can  remove  the  causes  of  error  that  have  been  pointed  out  by 
experience."  For  example,  it  would  be  imprudent  to  use 
mallein  in  case  of  animals  already  suffering  with  an  abnormally 
high  or  low  temperature.  The  further  precautions  should  be 
taken  that  the  animals  subjected  to  the  test  are  removed  as  far 
as  possible  from  atmospheric  variations  and  the  influence  of 
strong  sunlight,  fog.  rain  and  currents  of  air.  If  it  be  true 
that  the  majority  of  horses  are  not  susceptible  or  slightly  so, 
to  these  influences,  there  are  still  some  that  are  affected  by 
them.  A  rise  of  1.5  or  2  degrees  in  temperature  would  not 
necessarily  indicate  a  reaction.  Again,  it  must  not  be  for- 
gotten that  certain  diseases,  strangles  for  instance,  frequently 
produce  great  daily  variations  in  the  temperature  ;  therefore, 
when  there  is  reason  to  believe  in  the  presence  of  a  disease  of 
this  kind,  it  is  necessary  to  make  sure  that  the  increase  of 
temperature  consequent  on  injection  of  mallein  is  persistent, 
and  that  the  organic  reaction  is  clearly  present. 

Tlic  agglutination  method  or  serum  diagnosis.  Rabieaux 
found  tliatthe  difference  which  exists  between  the  agglutinat- 
ing power  of  a  serum  from  a  glandered  and  from  a  healthy 
horse  may  be  used  as  the  basis  of  a  method  or  diagnosing 
glanders.  He  collected  the  serum  as  pure  as  possible,  diluted 
it  with  sterile,  distilled  water  to  i  in  10,  or  to  i  in  500.  The 
diluted  serum  was  then  mixed  in  a  small  sterile  tube  with 
an  equal  volume  of  a  24  to  72  hour  culture  of  Bad.  mallei  in 
peptonized  bouillon  (without  glycerine).  The  mixture  was 
placed  in  an  incubator  at  a  temperature  of  35°  to  37°  C.  and 
examined  at  variable  times  under  the  microscope.  In  dilu- 
tions of  from  I  in  10  to  i  in  50  the  agglutination  occurred  in 
20  minutes  to  3  hours.  In  serum  of  a  non-glandered  horse 
from  2  to  6  hours  were  required  to  produce  the  agglutination. 
In  weaker  dilutions  the  differences  were  more  marked.  The 
development  of  the  method  can  be  followed  from  the  writings 
of  M'Fadyean,  Bourget  and  Mery,  Arpad,  Fedorowsky, 
Reinecke,  Bonome,  Schiitz  and  Miessner,  Schniirer  and 
Moore,  Tavlor  and  Giltner. 


MALLEIN  169 

The  method  consists  in  the  preparation  of  a  test  fluid  from 
a  suitable  culture  of  Bad.  mallei  to  which  is  added  the  diluted 
serum. 

The  "test- fluid"  is  prepared  by  washing  the  growth 
from  a  72  hour  acid-agar  culture  by  the  aid  of  a  sterile  wire 
loop  into  distilled  water  containing  0.85  per  cent  sodium 
chloride  and  0.5  per  cent  carbolic  acid  crystals.  This  suspen- 
sion is  then  placed  in  a  thermostat  at  60°  C.  for  two  hours, 
which  kills  the  bacteria.  Three  cubic  centimeters  of  the 
"test-fluid"  are  placed  in  each  of  several  small  test-tubes. 
With  a  sterile  pipette,  the  diluted  serum  is  added  to  the  tubes 
of  test-fluid  and  thoroughly  mixed.  In  making  the  different 
dilutions,  the  amount  of  diluted  serum  to  be  used  is  readily 
ascertained  by  the  following  table  : 


Dilution 

of  Amount  of  Di-' 

Amount 

of 

Dilution 

Serum 

luted  vSerum 

Test  Fluid 

1-40 

1.2       c.  c. 

3  c.  c. 

I-IOO 

1-40 

0.6 

3 

1-200 

1-40 

0.405 

3 

1-300 

1-40 

0.3 

3 

1-400 

1-40 

0  24 

3 

1-500 

1-40 
1-40 

0.195 
015 

3 

I -boo 
1-800 

1-40 

0.12 

3 

1-1,000 

1-40 

0.105 

3 

1-1.200 

1-40 

0.09 

0 

1-1,500 

1-40 

0.06 

3 

1-2,000 

1-40 

0.03 

3 

1-4,000 

1-40 

1      0.015 

1          3 

Where  dilutions  greater  than  i-iooo  are  made,  a  serum 
diluted  1-80  may  be  used  to  better  advantage,  unless  the 
pipette  employed  is  very  finely  graduated.  In  this  case  the 
amount  of  diluted  serum  for  a  certain  dilution  must  be  double 
that  indicated  in  the  table. 

The  mixture  thus  prepared  is  placed  in  an  incubator  at 
-,7°  C.  for  24-30  hours.  A  temperature  higher  than  37°  C. 
interferes  with  the  agglutination. 

The  reaction  consists  of  a  layer  of  the  agglutinated  bac- 
teria covering  the  entire  convexity  at  the  bottom  of  the  ttibe. 


lyo  GLANDERS 

This  film-like  sediment  may  become  so  dense  that  it  rolls  in  at 
the  periphery.  The  supernatant  fluid  becomes  clear  in  the 
lower  dilutions,  but  in  the  higher  ones  the  clarification  may 
not  be  complete,  showing  that  all  the  bacteria  have  not 
become  agglutinated.  This  is  further  evidenced  by  the  fact 
that  the  layer  is  less  dense  in  the  higher  dilutions.  The 
reaction  may  begin  in  six  hours,  but  cannot  be  considered 
complete  until  24  to  36  hours  have  elapsed.  If  no  reaction 
appears  in  24  hours  it  cannot  be  considered  negative,  as  it  may 
occur  in  from  30  to  40  hours  after  setting.  Often,  however,  a 
reaction  appears  in  less  than  24  hours. 

After  the  agglutination  is  completed,  further  standing 
produced  no  visible  change  in  the  test  fluid. 

A  negative  result  shows  a  small  round  concentrated  spot 
of  sediment  in  the  center  of  the  convexity  at  the  bottom  of  the 
tube,  the  test  fluid  remaining  apparently  unchanged  even  after 
several  weeks.  Animals  whose  blood  serum  agglutinates  in 
dilutions  of  1-500  are  suspicious  and  a  reaction  in  dilutions  of 
1-800  or  higher  indicates  an  infection  with  Bad.  mallei. 

As  pointed  out  by  Bononie  and  confirmed  by  Taylor, 
there  seems  to  be  little  or  no  change  produced  in  the  precipita- 
ting power  of  the  serum  of  the  blood  taken  before,  during  or 
after  the  mallein  reaction  but  the  agglutinating  power  as  deter- 
mined microscopically  is  very  much  increased  during  the 
mallein  reaction. 

This  is  shown  by  the  appended  table  : 


MALLEIN  171 

Table  showing  both  tnacroscopically  and  microscopially  the  ag^lulina- 

tion  of  dead  glanders  bacteria  with  blood  serum  from  horses 

taken  before,  during  and  after  the  mallein  reaction. 


Blood   taken  the     day    pre-  Blood   taken  during    Blood  taken  after  the 
vious   to  malleination  the  reaction  temperature  had  re- 

Feb.  21.  Feb.  22.  turned  to  normal 

.Mar.  2. 


V   1 

Macro- 

Micro-    1 

Macro- 

Micro- 

Macro- 

Micro- 

No.   1 

scopic 

scopic 

scopic 

scopic 

scopic 

scopic 

~T'\ 

1-800 

I-IOOO 

1-800 

1-1800 

1-800 



l-IOOO 

4 

1-800 

I - 1 200 

I-IOOO 

1-2000 

I-IOOO 

1-1500 

5 

1-1500 

I- J  600 

I-I500 

1-2500 

I-IOOO 

I-I200 

6 

I- 1 200 

1-1500 

I -1 200 

1-2000 

i-i8oo 

1-1800 

7 

I- 1000 

I- 1 200 

I - 1 000 

1-1800 

i-tooo 

I- I 400 

8 

1-500 

1-500 

I -800 

1-1600 

1-500 

1-600 

9 

1-800 

I-IOOO 

1-800 

1-1400 

1-500 

1-800 

10 

1-500 

1-600 

1-500 

I-IOOO 

1-500 

1-800 

12 

1-200 

1-300 

1-500 

1-800 

1-500 

1-750 

13 

I-IOOO 

I-I200 

1-500 

I-IOCO 

1-800 

I-IOOO 

14 

1-500 

1-600 

1-500 

1-800 

1-500 

1-800 

15 

1-1200 

I-I4OO 

1-1200 

1-2500 

1-1200 

I- I 800 

16 

I-IOOO 

I- I  200 

I-IOOO 

1-2400 

I-IOOO 

1-2200 

17 

1-500 

1-800 

1-800 

I -1500 

1-800 

I-I400 

18 

I-IOOO 

I-I400 

I-IOOO 

I-I800 

1-800 

I-I500 

19 

I-IOOO 

I-IOOO 

1-800 

1-1200 

I-IOOO 

I -I 200 

20 

1-500 

I-6GO 

1-500 

1-800 

1-500 

1-800 

21 

1-500 

1-750 

1-500 

I-IOOO 

1-800 

I-I200 

22 

I-IOOO 

I-I400 

I-IOOO 

1-2500 

1-800 

1-2200 

23 

1-200 

1-200 

1-200 

I-IOOO 

i~8oo 

I-IOOO 

24 

I-IOOO 

1-1200 

I-IOOO 

1-2200 

I- 1 200 

1-2000 

25 

1-800 

1-800 

1-500 

I- 1 200 

1-800 

I-IOOO 

26 

I- 1 200 

I-I500 

I-IOOO 

1-2200 

I- 1 200 

1-2000 

27 

1-500 

I-IOOO 

I-IOOO 

I-I800 

1-800 

1-2000 

28 

1-500 

1-600 

1-500 

I-I200 

I-IOOO 

1-1500 

29 

1-800 

I-IOOO 

1-500 

1-1200 

I-I200 

1-2000 

30 

I-IOOO 

I-I200 

1-800 

1-1800 

1-800 

1-1600 

31 

1-500 

1-600 

1-800 

1-1400    ' 

l-IOOO 

I-I500 

The  agglutination  in  higher  dilutions  with  the  living 
organisms  as  determined  microscopically  was  pointed  out  by 
Taylor.  A  comparison  of  the  agglutination  of  the  living  and 
killed  bacteria  with,  the  serum  from  glandered  horses,  as 
shown  by  the  mallein  reaction,  is  given  in  the  appended  table  : 


172 


GLANDERS 


Macroscopic  and  microscopic  agglutination  of  Bacterium  mallei  ivitli 
horse  serum  by  the  use  of  killed  atid  living  cultures. 


Number 

of 
Horse 

Macroscopic. 

Dead  bacteria,  24 

hours  at  37°  C. 

Microscopic. 

Dead  bacteria,  12 

hours  at  37°  C. 

Microscopic. 

Ivive  bacteria,  12 

hours  at  37°  C. 

I 

1-8000 

1-12000 

1-30000 

2 

1-2000 

1-3000 

1-12000 

3 

4 

1-800 
1-1600 

I-IOOO 

1-1800 

I-IOOOO 

1-6000 

5 
6 

7 
8 

9 

lO 

1-500 

I-IOOO 

i-Soo 
1-800 
1-1600 
1-500 

1-600 
I- 1 250 

I-IOOO 
I-I200 
I- 1800 
T-800 

1-5000 

1-25000 

1-8000 

I -1 2000 

1-24000 

1-7500 

The  method  as  pointed  out  by  Schiitz  and  Miessner  is  a 
macroscopic  one.  It  depends  upon  the  precipitation  ot  the 
agglutinated  masses  of  bacteria.  Normal  horse's  serum 
agglutinates  glanders  organisms  in  high  dilutions  as  deter- 
mined microscopically.  This,  however,  does  not  appear  to  be 
of  diagnostic  value. 

Disposition  of  reacting  horses.  The  question  arises 
whether  animals  found  by  the  help  of  mallein  or  the  agglutin- 
ation test  to  be  glanderedought  tobe  immediately  slaughtered. 
Nocard  said  no.  The  experience  of  the  last  few  years  goes  to 
prove  that  among  the  animals  that  react  there  are  some  which, 
when  removed  from  the  infected  center  and  thereby  withdrawn 
from  all  chance  of  new  contamination,  recover.  "We  ought 
therefore,"  he  continues,  "to  confine  ourselves  to  the  destruc- 
tion of  those  which  in  addition  to  the  reaction,  present  some 
clinical  indication  of  the  disease,  such  as  ulceration  of  the  nose, 
indurated  glands,  suppurative  lymphatics  or  other  pronounced 
manifestation  of  the  disease.  The  animals  showing  physical 
signs  of  infection  must  simply  be  removed  from  among  the 
healthy  horses  and  subjected  from  time  to  time,  say  every  two 
months,  to  the  mallein  test.  If  any  of  these  should  eventually 
show  the  clinical  signs  of  glanders,  it  should  be  slaughtered 
at  once.  On  the  other  hand,  those  animals  which  have  stood 
two  successive  doses  of  mallein  without  reacting  ought  to  be 


prevp:xtion  173 

considered  definitely  cured,  restored  to  their  places  and  put  to 
the  free  disposal  of  the  owners.'' 

The  views  advocated  by  Nocard  are  not  universally  enter- 
tained in  this  country.  It  has  been  shown  repeatedly  that  a 
good  reaction,  following  the  injection  of  mallein,  was  a  sure 
indication  of  glanders  as  revealed  by  post-mortem.  The 
question,  however,  concerning  the  necessity  of  immediate 
slaughter  for  purposes  of  protection,  where  there  are  no  evi- 
dences of  lesions  on  physical  examination,  seems  to  be  an  open 
one.  This  question  which  pertains  to  sanitary  police  rests, 
until  the  results  of  conclusive  investigations  are  recorded,  with 
those  entrusted  with  the  protection  of  animals  and  men  from 
this  disease.  However,  the  results  of  certain  experiments  in 
the  use  of  mallein  as  a  therapeutic  agent  and  the  fact  that  cer- 
tain animals  recover  when  kept  in  quarantine  are  very  sugges- 
tive. Certainly  further  investigations  are  needed  to  deter- 
mine the  safe  and  equitable  disposition  of  animals  devoid  of  all 
symptoms  and  obvious  lesions  of  glanders,  but  which  give  a 
reaction  to  the  mallein  or  agglutination  test. 

§  136.  Prevention.  Isolation  of  the  healthy  animals 
from  the  infected  ones  and  thorough  disinfection  of  the  stable 
are  important.  It  is  also  desirable  not  to  bring  strange  horses 
in  close  contact  with  home  animals,  until  their  freedom  from 
this  disease  is  determined. 

REFERENCES. 

1.  Babes.  Observations  sur  la  morve.  Arch,  de  Med.  e.vpcr.  et 
(/'  Anal,    path..   Vol.  Ill  (1891),  p.  619. 

2.  Berxs  and  Way.  Practical  Application  and  Results  of  the 
Agglutination  Method  of  Diagnosing  Glanders  in  One  Hundred  and 
Fifty-two  Cases.      Amer.  Vet.  Rev.,  Vol.  XXX  (1906),  p.  822. 

3.  BONOME.  Leber  die  Schwankungen  des  Agglutinin  und 
Prazipitingehaltes  des  Blutes  wahrend  der  Rotzinfektion,  Centralbl.  f. 
Bakt.,  Bd.  XXXVIII.  (1905^  S.  601. 

4.  BouRGET  ET  Mern'.  Sur  le  seradiagnostique  de  la  morve,  La 
Semaine  Med.,  1898,  p.   61. 


174  GLANDERS 

5.  Butler.  Glanders.  Bulletin  A^o.  /6.  J/tss.  Agr.  Exp.  Sta- 
tion, iSgi. 

6.  Carv.  Glanders.  Bulletin  No.  jj;.  Ala.  Agr.  Expt.  Station 
of  the  Agricultural  and  Jlechanical  College,  Jan.   1892. 

7.  Dawson.  Equine  glanders  and  its  eradication.  Bulletin  No. 
77.     Florida  Agric.  Exp.  Station,  1905. 

8.  De  Schweinitz  and  Kilbornh.  The  use  of  mallein  for  the 
diagnosis  of  glanders  in  horses  and  experiments  with  an  albumose 
extracted  from  cultures  of  bacillus  mallei.  Am.  Vet.  Revieic,  Vol. 
XVHiS92),p.  439. 

9.  Francis.  Glanders,  tests  with  mallein.  Bulletiti  No.  jo. 
Texas,  Agri.  Exp.  Station,  1894. 

10.  Frothingham.  The  diagnosis  of  glanders  by  the  Strauss 
method.    Jour,  of  ISIedical  Research,     Vol.  VI  ( 1901 ),  p.  331. 

11.  Galli-Valhrio.  Contribution  a  1' etude  de  la  morphologic 
du  Bacillus  mallei.     Centralb.    fiir  Bakt.,  Bd.  XXVI  (1899).  S.  177. 

12.  HiGGiNS.  Glanders  and  mallein.  Proceedings  Atner.  Vet 
Med.  Asso.,  1904,  p.  135. 

13.  LfANGER.  Untersuchuug  iiber  die  differential  diagnostische 
Bedeutung  der  Rotzagglutination  u.  s.  w.  Afonatshefte  fiir  prak. 
Tierheilkunde,  Bd.  XVI  (1905),  vS.  241. 

14.  Loeffler  and  Schutz.  On  the  bacillus  of  glanders.  Deutsche 
Med.  Wochenschrift,  Dec.  1882.  Translated,  Vol.  CXV,  New  Sydenham 
Society. 

15.  M'Fadvean.  The  pulmonary  lesions  of  glanders.  Jour,  of 
Compar.  Path,  and  Thera.,  Vol.  VIII  (1895),  p.  50. 

16.  M'Fadyean.  Glanders.  Jour.  Compar.  Path,  and  Thera., 
Vol.  XVII  (1904),  p.  295. 

17.  Moore,  Taylor  AND  GiLTNER.  The  Agglutination  Method 
for  the  Diagnosis  of  Glanders.  Avier.  Veter.  Rev.,  Vol.  XXX 
(1906),  p.  803. 

18.  NocARD.  The  value  of  mallein  as  a  means  of  diagnosis  in 
doubtful  cases  of  glanders.  Jour.  Compar.  Path,  and  Thera.,  Vol.  VIII 
(1895),  p.  227. 

19.  Rabieacx.  Serum  diagnosis  of  glanders.  Abstract  Jour. 
Compar.  Path,  a ?id  Thera.,  Vol.  XVI  (1903),  p.  59.  Orig.  Jour,  de 
Med.  Vet.,  1902. 

20.  Reynolds.  State  control  of  glanders  in  Minnesota.  Jour,  of 
Compar.  Med.  and  vet.  Archives,  Vol.  XX  (1899). 

21.  Rutherford.  Glanders.  Proceedings  Am.  Vet.  Med.  Asso., 
1906,  p.  215. 


TUBERCULOSIS  1 75 

22.  SCHi'TZ.  A  contribution  to  the  subject  of  jflaiulers.  Jour,  of 
Compar.  Path,  and  Thrra  ,  Vol.  XI  (1898),  p.  i. 

23.  SCHUTz.  Zur  Lehre  voni  Rot/.e.  .Iniiii.fur  ?ciss.  11.  prakt. 
T/iierheilkunke,  Bd.  XXIV  (1898),  S.    i. 

24.  SCHiJTZ  UND  MiESSNER.  Zur  Serodiagnose  der  Rolzkranklieit. 
Archiv.fih-   K'iss.  u.  prakt.  Ticrliielkunde,  Bd.  XXXI  (1905),  S.  353. 

25.  Smith.  On  the  influence  of  slight  modifications  of  culture 
media  on  the  growth  of  bacteria  as  illustrated  by  the  glanders  bacillus. 
Journal  of  Comparative  Medicine,  (1890),  p.  158. 

26.  Strong.  Preliminary  report  of  the  appearance  in  the  Philip- 
pine Islands  of  a  disease  clinically  resembling  glanders.  1902,  No.  /, 
Bureau  of  Government  Laboratories,  Manila. 

27.  Strauss.  Sur  un  moyen  diagnostique  rapide  de  la  morve. 
Arch,  de  Med.  e.vper.  et  de  Anat.  path.,  Vol.  Ill  ( 1889),  p.  460. 

28.  Way.  The  practical  application  of  the  agglutination  method 
for  the  diagnosis  of  glanders.  Am.  I'ct.  Revicxv,  Vol.  XXXI 
(1907),  p.  709. 

29.  Wherrv.  Glanders  :  Its  diagnosis  and  Prevention.  Bulletin 
No.  24.     Bureau  of  Government  Laboratories.     Manila.     (1904). 

30.  Williams.   Glanders.    Bui.  No.  4.  Mont.  Agr.  Exp.  Stat.,  1894. 

31.  Wright.  The  histological  lesions  of  acute  glanders  in  man 
and  of  experimental  glanders  in  the  guinea  pig.  Jour,  of  Exp.  Med., 
Vol.  I  (1896),  p.  577. 


TUBERCULOSIS 


Synonyms.  Consumption  ;  pearl  disease  ;  grapes;  phthisis  ; 
scrofula  ;  tabes  ;   "The  great  white  plague." 

§  137,  Characterization.  Tuberculosis  is  an  infectious 
disea.se  from  which  the  human  .species,  cattle  and  swine  suffer 
very  exten.sively  and  which,  under  favorable  conditions,  attacks 
nearly  if  not  all  species  of  animals  including  fish.  It  is  a  dis- 
ease of  slow  development,  involving  either  primarily,  or  in 
association  with  other  organs,  the  lymphatic  system.  It  is 
characterized  by  the  formation  of  nodules,  or  tubercles,  in 
consequence  of  the  activities  of  Bacterium  tuberculosis.  It  does 
not  destroy  life  by  acute  toxemia,  but  by  a  chronic  and  Umg 
continued  systemic  poisoning  and  by  the  morbid  changes 
brought  about  through  the  localization  of  these  lesions  in 
organs  necessary  to  life. 


176  TUBERCULOSIS 

§  138.  History.  Tuberculosis  is  one  of  the  oldest  dis- 
eases affecting  cattle  of  which  there  are  identifying  records. 
It  seems  to  have  been  known  to  the  Jewish  people  during  their 
Egyptian  captivity  and  the  ecclesiastical  laws  for  many  cen- 
turies contained  numerous  enactments  against  the  consump- 
tion of  flesh  from  tuberculous  animals.  In  1370,  it  was  for- 
bidden in  Munich  to  have  on  sale  the  flesh  of  animals  affected 
with  tuberculosis.  A  number  of  other  cities  passed  similar 
ordinances.  In  1702,  Florinus  described  the  disease  and 
emphasized  the  then  existing  opinion  that  it  was  identical  with 
syphilis.  This  led  to  the  practice  of  destroying  all  tubercu- 
lous animals.  In  1783,  the  Berlin  Board  of  Health  rejected 
the  theory  of  the  connection  of  tuberculosis  and  syphilis  and 
declared  the  flesh  of  affected  animals  to  be  fit  for  food.  This 
led  finally  to  the  cancelling  of  all  laws  throughout  Prussia 
against  the  use  of  flesh  for  food  trom  animals  affected  with  the 
disease.  Tscheulin,  in  1816,  recognized  in  reference  to  the 
infection  of  meat,  three  degrees  of  bovine  tuberculosis,  viz: 
I,  in  which  the  tubercles  were  to  be  removed  ;  2,  in  which  the 
diseased  parts  were  to  be  destroyed  and  the  meat  sold  at  a  low 
price  ;  and  3,  those  cases  in  which  the  lesions  were  so  exten- 
sive that  the  whole  carcass  must  be  rejected. 

The  study  of  the  lesions  themselves  gave  rise  to  a  num- 
ber ot  beliefs  concerning  their  nature.  Thus,  Virchow,  Schup- 
pel  and  others  declared  that  the  tubercles  in  cattle  were  lym- 
pho-sarcomata.  L,eisering  considered  them  simply  as  sarco- 
mata. Spinola  and  Haubner  maintained  that  human  and 
bovine  tuberculosis  were  identical. 

In  1865,  Villemin  showed  that  tuberculosis  was  due  to  a 
specific  infection.  He  produced  the  disease  in  rabbits  by 
inoculating  them  with  tuberculous  material  from  human  sub- 
jects. He  also  produced  the  disease  by  feeding  experimental 
animals  and  by  causing  them  to  inhale  tuberculous  material. 
Chauveau,  in  the  same  year,  produced  the  disease  in  cows. 
These  results  were  soon  confirmed  by  Klebs,  Cohnheim  and 
Gerlach.  These  experiments,  in  which  the  disease  was  pro- 
duced in  one  species  with  tuberculous  material    from    another, 


HISTORY  177 

followed  by  the  discovery  by  Koch  of  the  specific  bacterium  of 
the  disease,  led  to  the  view  that  tuberculosis  in  all  species  of 
mammals  was  identical.  This  generally  accepted  belief  caused 
sanitarians  to  look  upon  tuberculosis  in  cattle  as  a  great  men- 
ace to  public  health.  The  result  was  that  during  the  closing 
decade  of  the  last  century,  this  disease  in  cattle  was  treated 
more  vigorously  as  a  menace  to  the  human  species  than  as  a 
destructive  disease  of  animals. 

In  1896,  Dr.  Theobald  Smith  pointed  out  that  for  certain 
animals  the  tubercle  bacteria  from  cattle  were  more  virulent 
than  those  from  man  and  further  that  there  were  certain 
morphological  and  cultural  differences  existing  between  them. 
In  1898,  he  published  the  results  of  a  more  extended  series  of 
investigations.  Since  that  time  a  number  of  investigators 
have  arrived  at  the  same  conclusion.  The  fact  has  come  to  be 
well  known  that  certain  differences  exist  between  the  bacteria 
of  tuberculosis  found  in  the  human  and  in  the  bovine  species. 
Koch's  experiments  reported  at  the  tuberculosis  congress  in 
London  in  July,  1901,  give  additional  evidence  of  a  difference 
in  virulence  for  experimental  animals  of  the  bacteria  of  human 
and  of  bovine  tuberculosis.  To  what  extent  the  human 
species  becomes  infected  from  the  bovine  kind  cannot  be 
stated,  but  the  accumulating  evidence  tends  to  the  conclusion 
that  bovine  tuberculosis  is  of  less  significance  in  its  influence 
upon  public  health  than  has  heretofore  been  thought,  and  ol 
more  importance  as  a  rapidly  spreading  and  destructive  dis- 
ease among  cattle.  It  is  not  proven,  however,  that  the  human 
species  is  not  affected  with  the  bacteria  of  bovine  tubercu- 
losis. The  investigations  of  the  last  five  years  have  shown 
that  not  infrequently  human  tubercle  material  will  produce 
tuberculosis  in  cattle.  The  interim  reports  of  the  Royal  Com- 
mission appointed  in  1901  are  important  in  this  connection. 
Salmon  has  published  an  important  paper  on  the  relation  of 
human  and  bovine  tuberculosis  in  reply  to  Koch's  paper  of 
1 90 1.  Concerning  its  transmission,  the  conclusion  seems  to  be 
warranted,  that  the  virus  of  tuberculosis  spreads  very  largely 
among  men  and  cattle  from    individual    to    individual    of    the 


178  TUBERCULOSIS 

same  species  rather  than  from  one  species  to  the  other.  A 
number  of  cases  of  tuberculosis  in  mau  seems  to  have  been 
caused  by  the  bovine  type  of  the  tubercle  bacterium.  Accord- 
ing to  Smith  there  are  forty  to  fifty  such  cases  on  record. 

§  139.  Extent  of  tuberculosis  especially  among 
cattle  and  swine.  The  committee  on  cattle  diseases  and 
animal  food  of  the  American  Public  Health  Association  for 
1901  reported  the  appended  statistics  concerning  the  extent  and 
increase  of  tuberculosis  in  cattle  and  swine  in  various  countries. 

"The  slaughter  house  statistics  of  Prussia  show  14.6  per 
cent  of  the  cattle  and  2. 14  per  cent  of  the  swine  to  be  tubercu- 
lous. In  Saxony  the  percentage  is  29.13  with  cattle  and  3.10 
with  swine.  In  the  city  of  Leipzig  the  figures  are  36.4  for 
cattle  and  2. 17  for  swine  (Siedamgrotzky).  Of  20,850  animals 
in  Belgium  tested  with  tuberculin  in  1896,  48.88  per  cent 
reacted.  Of  25,439  tested  in  Denmark  from  1893  to  1895, 
49.3  per  cent  reacted  ;  and  of  67,263  tested  from  1896  to  1898, 
32.8  per  cent  reacted  (Bang).  An  examination  of  20,930 
cattle  in  Great  Britain,  either  slaughtered  and  examined  post- 
mortem or  tested  with  tuberculin,  showed  5,441  or  26  per  cent 
affected  with  tuberculosis.  M'Fadyean  estimates  that  30  per 
cent  of  the  cows  !n  Great  Britain  are  tuberculous.  Figures 
available  in  the  United  States  do  not  cover  a  sufficient  area  of 
our  territory  to  allow  us  to  make  a  reliable  estimate  of  the 
extent  of  tuberculosis  in  milch  cows. 

"Our  beef  cattle  as  they  come  to  the  large  packing  houses 
are  as  yet  comparatively  free  from  tuberculosis.  Of  4,841,166 
cattle  slaughtered  in  the  year  1900,  under  Federal  meat  inspec- 
tion, but  5,279  or  o.  II  per  cent  were  sufficiently  affected  to 
cause  the  condemnation  of  any  part  of  the  carcass.  Of  23,336,- 
884  hogs  similarly  inspected,  5,440  were  sufficiently  affected  to 
cause  a  condemnation  of  some  part  of  the  carcass.  This  is 
equal  to  0.023  per  cent,  or  slightly  more  than  one-fifth  the 
proportion  found  in  beef  cattle. 

"The  slaughter  house  statistics  of  all  countries  show  that 
the  percentage  of  affected  hogs  increases  as  the  disease  becomes 


GEOGRAPHICAL    DISTRIHUTION  179 

more  common  in  cattle,  so  that  we  must  consider  not  only  the 
effect  of  the  disease  upon  beef  and  milk  producing  animals 
but  also  upon  swine.  Tuberculosis  is  more  acute  with  hogs 
than  with  cattle,  and  there  is  a  much  greater  tendency  to  gen- 
eralization, consequently  the  parts  used  for  human  food  are 
more  likely  to  be  affected,  and  if  there  is  a  possibility  of  com- 
municating the  virus  through  the  meat  the  danger  is  increased 
by  this  peculiarity  of  the  disease  in  swine."  The  statistics  of 
the  last  few  years  show  a  rapid  increase  in  the  amount  of 
tuberculosis  in  swine.  In  1905  64,919  carcasses  of  hogs  and 
142,105  parts  were  condemned  for  tuberculosis. 

Ji  140.  Geographical  distribution.  Tuberculosis  is  an 
exceedingly  wide  spread  disease.  In  earlier  times  it  was  quite 
prevalenramong  cattle  in  Central  Europe.  It  seems  to  have 
existed  in  Western  Asia  and  Northern  Africa  at  an  early  date. 
From  these  centers  it  has  spread  to  nearly  every  cattle  raising 
country  of  the  world.  Its  rapid  spread  during  the  last  fifty 
years  is  attributed  to  the  increase  in  cattle  exchange  resulting 
in  the  introduction  of  tuberculous  animals  into  healthy  herds. 
It  is  stated  that  in  many  countries,  and  in  large  districts  with- 
in others,  tuberculosis  did  not  exist  until  it  was  introduced 
within  recent  years  by  the  importation  of  diseased  animals. 

In  countries  where  there  has  been  little  or  no  importation 
of  cattle  and  in  which  the  native  breeds  still  exist  unchanged, 
as  in  manv  parts  of  Russia,  Austria  and  Spain,  in  the  north- 
ern part  of  Sweden  and  Norway,  and  in  parts  of  Africa,  tuber- 
culosis is  practically  unknown.  This  is  true  of  the  cattle  on 
the  island  of  Jersey,  where  for  more  than  a  hundred  years  for- 
eign cattle  have  not  been  introduced. 

In  the  United  States,  the  disease  is  very  widely  distrib- 
uted It  is  found  to  a  considerable  extent  in  certain  localities 
where  the  climatic  conditions  seem  to  be  beneficial  for  tubercu- 
lous people.  The  explanation  for  this  seems  to  be  that  tuber- 
culous animals  have  been  introduced  into  certain  herds  in  these 
districts  There  are,  however,  large  areas  in  which  it  is  prac- 
ticallv  unknown.     The  Western  steers  that  are   killed  in  the 


i8o 


TUBERCULOSIS 


slaughter  houses  of  Kansas  Cit}^  Omaha,  Sioux  City  and 
Chicago  are  practically  free  from  this  disease.  Tuberculosis 
exists,  however,  in  many  places  where  beef  cattle  are  raised,  as 
the  result  of  the  introduction  of  affected  breeding  stock.  In 
many  localities,  especially  where  there  is  an  extensive  inter- 
change of  animals,  a  large  percentage  of  the  herds  are  more  or 
less  affected. 

§  141.  Etiology.  Tuberculosis  is  caused  by  a  rod- shaped 
organism  known  as  Bacterium  tuberculosis.  It  was  discovered 
by  Robert  Koch  in  1882.  Schiil- 
ler  and  Toussaint  had  previously 
studied  growths  which  seem,  from 
the  results  of  their  inoculation  ex- 
periments, to  have  been  this  organ- 
ism. The  bacterium  of  tuberculosis 
is  a  slender,  rod-shaped  organism 
with  rounded  ends,  from  2  to  5/<  in 
length  and  from  0.3  to  o.5/<  broad. 
The  rods  are  straight  or  slightly 
curved,  and  occur  singly,  in  pairs 
or  in  small  bundles.  Frequently 
they  cross  one  another.  They  do 
not  produce  spores,  but  vacuoles  are  often  observed  and 
branching  forms  have  been  described. 

The  bacterium  of  tuberculosis  is  readily  cultivated  on 
artificial  media  such  as  blood  serum,  glycerinated  agar  and 
bouillon  after  it  has  been  adapted  to  such  artificial  conditions.* 
It  is,  however,  not  easy  to  cultivate  it  directly  from  ordinary 


Fig.  30. 


Bacterium  tuber- 
culosis. 


*To  accomplish  this  necessitates  a  very  special  and  careful  proce- 
dure. Dr.  Theobald  Smith,  of  Harvard  University  (Jour  of  Exp.  Med., 
Vol.  III.,  1898,  p.  451),  has  the  credit  of  formulating  a  method  by  com- 
bining details  in  such  a  manner  that  the  procuring  of  cultures  is,  in 
most  cases,  possible.  Dog  serum  is  used.  The  method,  as  he  gives  it, 
is  as  follows  : 

"  The  dog  was  bled  under  chloroform  and  the  blood  drawn  from  a 
femoral  artery,  under  aseptic  conditions,  through  sterile  tubes  directly 
into  sterile  flasks.  The  serum  was  drawn  from  the  clots  with  sterile 
pipettes  and  either  distributed  at  once  into  tubes  or  else  stored  with  0.25 


ETIOLOGY  IS  I 

tuberculous  lesions.  Although  at  the  time  of  their  discovery, 
the  tubercle  bacteria  from  man  and  from  animals  were  believed 
to  be  identical,  they  have  been  found  to  possess  slightly  differ- 
ent characters  and  properties.  Smith  pointed  out  in  1898, 
that  morphologically  those  from  cattle  wereshorter  and  thicker 
than  those  from  man,  that  the  growth  was  slightly  different 
on  blood  serum,  and  that  they  were  much  more  virulent  for 
cattle  and  rabbits  than  those  from  the  human  species.  Since 
that  time  his  conclusions  have  been  confirmed  by  a  number  of 
investigators.  Koch  obtained  like  results.  At  present,  there- 
fore, we  must  look  upon  the  tubercle  bacteria  coming  from 
these  different  species  as  possessing  races  or  varieties  which, 
perhaps,  are  the  result  of  their  different  conditions  of  life. 
The  investigations  which  have  been  made  with  the  decidedly 
different  forms  of  this  organism  found  in  tuberculosis  of  fowls 
and  of  fish  have  led  a  few  experimenters  to  believe  that  they 
are  simply  varieties  of  the  organism  first  described  by  Koch. 
Further  inquiries  are  necessary  to  fully  satisfy  bacteriologists 
that  all  of  these  forms  are  thus  related  to  the    one    species. 

to  0.3  per  cent  chloroform  added.  Discontinued  sterilization  was  ren- 
dered unnecessary.  The  temperature  required  to  produce  a  sufficiently 
firm  and  yet  not  too  hard  and  dry  serum  is  for  the  dog  75°  to  76° C.  For 
horse  serum  it  is  from  4°  to  5°  lower.  The  serum  was  set  in  a  thermo- 
stat into  which  a  large  dish  of  water  was  always  placed  to  forestall  any 
abstraction  of  moisture  from  the  serum.  About  3  hours  suffice  for  the 
coagulation.  When  serum  containing  chloroform  is  to  be  coagulated,  I 
am  in  the  habit  of  placing  the  tubes  for  an  hour  or  longer  in  a  water 
bath  at  55°  to  60°  C,  or  under  the  receiver  of  an  air  pump,  to  drive  off 
the  antiseptic.  This  procedure  dispenses  with  all  sterilization  excepting 
that  going  on  during  the  coagulation  of  the  serum.  It  prevents  the 
gradual  formation  of  membranes  of  salts,  which,  remaining  on  the  sur- 
face during  coagulation,  form  a  film  uusuited  for  bacteria.  Tubes  of 
coagulated  serum  should  be  kept  in  a  cold  closed  space  where  the 
opportunities  for  evaporation  are  slight.  They  should  always  be  kept 
inclined. 

"The  ordinary  cotton-plugged  test  tubes  I  do  not  use,  because  of 
the  rapid  drying  out  permitted  by  them,  as  well  as  the  opportunities  for 
infection  with  fungi.  Instead,  a  tube  is  used  which  has  a  ground  glass 
cap  fitted  over  it.  This  cap  contracts  into  a  narrow  tu])e  plugged  with 
glass  wool.     This  plug  is  not  disturbed.     The  tube  is  cleaned,  filled,  and 


1 82  TUBERCULOSIS 

There  seems  to  be  no  reason  for  doubting  that  the  bovine  and 
human  forms  are  varieties  or  races  of  the  same  species.  The 
diiTerence  in  the  conditions  of  life  under  which  they  exist  in 
the  bodies  of  men  and  of  cattle  are  quite  enough  to  explain 
resulting  differences  in  the  bacteria. 

S  142.  Symptoms.  The  symptoms  vary  according  to 
the  course  of  the  disease.  There  is  a  chronic  form,  which  is 
most  common,  and  an  acute  form  or  miliary  tuberculosis. 

The  symptoms  of  chronic  tuberculosis  depend  upon  the 
location  of  the  lesions  and  their  extent.  When  the  lesions  are 
situated  deeply  and  are  not  of  great  extent,  they  may  not 
exhibit  visible  evidence  of  their  presence.  In  such  cases,  the 
infected  animal  may  present  the  picture  of  perfect  health  and 
show  no  disturbance  of  function.  Indeed  some  animals,  in 
which  the  lesions  are  both  extensive  and  widely  distributed 
and  which  have  never  presented  noticeable  signs  of  the  disea.se, 
are  slaughtered  for  beef  without  a  suspicion  of  the  presence  of 
tuberculosis  until  they  are  examined  post- mortem. 

inoculated  by  removing  the  cap.  With  sufficient  opportunity  for  the 
interchange  of  air  little  evaporation  takes  place,  and  contamination  of 
the  culture  is  of  very  rare  occurrence.  In  inoculating  these  tubes,  bits 
of  tissue,  which  include  tuberculous  foci,  especially  the  most  recent, 
are  torn  from  the  organs  and  transferred  to  the  serum.  Very  little 
crushing,  if  any,  is  desirable  or  necessary.  I  think  many  failures  are 
due  to  the  often  futile  attempts  to  break  up  firm  tubercles.  Nor 
should  the  bits  of  tissue  be  rubbed  into  the  surface,  as  is  sometimes  rec- 
ommended. After  a  stay  of  several  weeks  in  the  thermostat,  I  usually 
remove  the  tubes  and  stir  about  the  bits  of  tissue.  This  frequently  is 
the  occasion  for  a  prompt  appearance  of  growth  within  a  week,  as  it 
seems  to  put  certain  still  microscopic  colonies  in  or  around  the  tissue 
into  better  condition  for  further  development.  The  thermostat  should 
be  fairly  constant,  as  urged  by  Koch  in  his  classic  monograph,  but  I 
look  upon  moisture  as  more  important.  If  possible,  a  thermostat  should 
be  used  which  is  opened  only  occasionally.  Into  this  a  large  dish  of 
water  is  placed,  which  keeps  the  space  saturated.  Ventilation  should 
be  restricted  to  a  minimum.  As  a  consequence,  moulds  grow  luxuri- 
antly and  even  the  gummed  labels  must  be  replaced  by  pieces  of  stiff 
manila  paper  fastened  to  the  tube  with  a  rubber  band.  By  keeping  the 
tubes  inclined,  no  undue  amount  of  condensation  water   can   collect  in 


SYMPTOMS 


183 


Since  the  lesions  of  tuberculosis  vary  so  much  in  different 
cases   it  is  not  possible  to  give  a   description   of   what  can  be 
designated  the  characteristic  or   even   the   usual  symptoms  ot 
this   disease.       There 
are,  however,   certain 
general    manifesta- 
tions  that  appear    in 
most  of  the  advanced 
cases,  such  as  emacia- 
tion while   the    appe- 
tite   continues    good. 
This  is  always  a  sus- 
picious indication  and 
especially    if    accom- 
panied   by     cough, 

rough  coat  and  tight, 

harsh   skin.       Rough 

or  loud   respiratory 

sounds  are  suspicious, 

and,   in    advanced 

cases,  it  is  often  found 

that  the  animal  groans 

when    pressure    is 

brought  to  bear  upon 

the  chest  wall.   Many 

cases  bloat  habitually. 

Hard,  painless  swel- 
lings (enlarged  lymp- 
hatic glands)  beneath 
the  skin  in  the  region 
of  the  escutcheon, 
flank,  shoulder  or  throat  are  .suspicious 


Fig.  31.  Right  lateral  aspect  of  posterior 
half  of  steer's  head,  {a)  Lower  jaw,  {b)  ear 
passage,  {c)  horn,  [d)  styloid  process  of 
occipital  bo7ie,  {e)  parotid  gland,  {J)  sub- 
ma  villary  gland.  A .  Right  parotid  lymph 
gland.  B.  Right  post  maxillary  lymph 
gland.  C.  Right  submaxillary  lymph 
gland.  These  glands  are  often  the  seat  oj 
'^tubercular  deposits  {Stnitli). 


thebotW^TI^  the  upper  portion  of  tl.e  ,eru„,  '"-^  ^  '^'^ 
only  precaution  to  be  applied  .0  prevent  ,n,ec„on  "'  '  "°"'^^  'g° 
.Jo     l,l,«a.^tbej^,.„.bet.ee„tu^ 

Llip'meTorenl^'th'rptu,  into  sterile  .ol.eu  para«in  an.!  .0  cover 


184  TUBERCULOSIS 

In  tuberculosis  of  the  luugs,  it  may  be  said  that  coughing 
is  the  most  noticeable  symptom.  It  is  most  common  after 
feeding,  drinking,  or  after  rapid  moving  following  a  period  ot 
repose,  but  sometimes  it  occurs  without  any  apparent  cause. 
The  cough  is  usually  strong,  dry  and  frequently  of  a  high 
pitch.  Sometimes  it  is  very  violent,  accompanied  by  protru- 
sion of  the  tongue.  Auscultation  reveals  modified  and  abnor- 
mal sounds  of  different  kinds  in  the  lungs  ;  sibilant,  sonorous 
and  mucous  rales  are  most  common.  A  dull  sound  is  often 
detected  on  percussion.  It  is  also  to  be  noted  that  this  condi- 
tion is  of  slow  development  and  long  duration,  thus  aiding  one 
to  distinguish  it,  in  many  cases,  from  bronchitis  or  pneumonia. 

Where  the  mediastinal  lymphatic  glands  are  enlarged  and 
press  upon  the  esophagus,  it  is  stated  that  the  animal  bloats 
habitually.  Chronic  or  habitual  bloating  accompanied  by  a 
good  appetite  and  no  other  evidence  of  disease  of  the  digestive 
tract,  especially  if  there  is  shortness  of  breath  and  cough, 
may  be  looked  upon  as  strongly  indicative  of  tuberculosis  with 
enlarged  mediastinal  lymphatic  glands.  Enlarged  tubercular 
glands  along  the  esophagus  may  press  upon  that  organ  caus- 
ing obstructions  and  preventing  the  escape  of  gases  from  the 
stomach.     This  often  gives  rise  to  lymphangitis. 

vSometimes  large  tubercular  masses  develop  on  the  pleura. 
In  such  cases  the  principal  symptom  is  a  friction  sound  that  is 
heard  most  distinctly  during  inspiration.  If  the  masses  are 
large  enough  they  give  rise  to  a  dull  sound  upon  percussion. 
In  tuberculosis  of  the  stomach  and  intestines,  digestion  is 
interfered  with.  This  gives  rise  to  poor  appetite,  frequently 
to  diarrhea  and  sometimes  to  alternation  of  diarrhea  and  con- 
stipation. In  tuberculosis  of  the  peritoneum  or  of  the  lin- 
ing of  the  abdominal  cavity,     the    lymphatic    glands    of    the 

the  tube  with  a  sterilized  paper  cap.     The  white  bottle  caps  of  the  drug- 
gist aje  very  serviceable." 

While  the  tuberculous  material  is  perfectly  fresh  (uncontaminated) 
and  in  the  early  stages  of  the  disease,  it  is  safer  to  inoculate  a  guinea 
pig,  and  after  the  lesions  begin  to  develop  to  chloroform  it  and  make 
the  cultures  from  the  recently  affected  liver  or  spleen. 


SYMPTOMS 


:85 


flank  are  often  enlarged  and  hard.  vSonietimes  this  condition 
can  be  diagnosed  positively  by  a  rectal  examination  and  the 
discovery  of  the  hard,  nodular  masses.  Tuberculosis  of  the 
liver  does  not  give  rise  to  obvious  symptoms  unless  the  dis- 
ease is  far  advanc- 
ed, in  which  case 
jaundice  may  be 
observed. 

In  animals    in 
which      the     post- 
pharyngeal      lym- 
phatic   glands    are 
enlarged    from    tu- 
berculosis,       the 
breathing  is  harsh 
and  noisy.     In  this 
condition    there   is 
sometimes  difficul- 
ty   i'n    swallowing, 
and    particles    o  f 
chewed  up  food  are 
occasionally  expel- 
led from  the  mouth, 
either     voluntarily 
when    it    is    found 
that  they  cannot  be 
swallowed  conven- 
iently,   or   by    the 
coughing  they  oc- 
casion upon  reach- 
ing   the    pharynx. 
These  enlarged 
glands  may    some- 
times  be    detected 
by  palpation  accomplished  by  placin 
of  the  throat  above  the  larynx  and    then  pressing   from    op 
posite  sides. 


Fig.  32.  Dorsal  aspect  of  bovine  lungs,  {a-a') 
right  and  left  caudal  lobes,  (b-b')  r.  and  I.  ven- 
tral lobes,  [c-C)  first  and  second  right  cephalic 
lobes,  {c^-)  left  cephalic  lobe,  {e)  trachea,  {x  x) 
region  most  frequently  involved  in  the  earliest 
stages  of  pulmonary  tuberculosis.  The  lesions 
at  this  stage  are  usually  embedded  in  the  lung 
tissue  {Smith). 

one  hand  on  each  side 


i86 


TUBERCULOSIS 


Tuberculosis  of  the  udder  is  detected  by  an  enlargement 
and  hardening  of  the  affected  part,  usually  by  the  absence  of 
f.  pain  and  the  fact  that  the 

secretion  is  not  altered  un- 
til the  part  has  been  dis- 
eased for  some  time.  In 
advanced  cases,  instead 
of  milk,  the  udder  se- 
cretes a  yellowish,  cloudy 
and  sometimes  flocculent 
liquid.  In  acute, 
rapidly  developing  cases, 
there  may  be  pain  and 
edema  of  the  skin.  In 
nearly  all  cases  of  udder 
tuberculosis  the  supra- 
mammary  lymphatic  glands 
situated  above  the  udder  in 
the  middle  of  the  escutch- 
eon, are  enlarged  and  hard. 
If  there  is  doubt  as  to  the 
character  of  the  disease  of 
the  udder,  the  milk,  or 
possibly  a  piece  of  excised 
udder  tissue,  may  be  ex- 
amined bacteriologically. 

In  tuberculosis  of  the 
brain,  the  animal  is  un- 
steady and  uncertain  in  its 
movements.  It  lies  down 
much  of  the  time,  is  usuallj^ 
subject  to  occasional  cramps 
and  is  apt  to  carry  the  head 
in  an  unusual  position. 
Such  cases  are  inclined  to 
advance  rapidly  and  termi- 
nate in  death  following  coma  or  convulsions. 


Fig.  33.  Trachea  and  bronchial  tubes, 
of  bovine  lungs  shoiving  attached 
bronchial  glands,  (a-a')  Supply  right 
and  left  caudal  lobes,  {b.b')  supply  r. 
and  I.  ventral  lobes,  {c-c')  branches  of 
the  right  supernumerary  bronchus, 
((C=)  supply  left  cephalic  lobe,  {d) 
branch  to  azygous  lobe,  {e)  trachea. 
A.  Left  bronchial  lymph  gland.  B. 
Right  bronchial  lymph  gland.  C. 
Lymph  gland  base  of  supranumerary 
bronchus.  D.  gland  often  betiueen 
bronchi.  The  glands  A.  to  D.,  are 
often  involved  {Smith). 


SYMPTOMS 


187 


In  tuberculous  disease  of  the  bones  and  joints,  the  parts 
are  enlarged,  there  is  loss  of  motion,  pain  and  usually  abscess 
formation  followed  by  the  discharge  of  thick  yellow  pus. 
In  tuberculosis   of 

the  uterus  or  ovar-  1 1  »   / 

ies  and  sometimes 
in  peritoneal  tuber- 
culosis of  the  cow, 
the  subject  is  al- 
most continually  in 
heat.  In  tubercu- 
losis of  the  uterus, 
there  is  sometimes  a 
discharge  of  thick, 
yellowish  material 
mixed  with  mucus. 
In  tuberculosis  of 
the  testicles  the  or- 
gans become  en- 
larged and  hard. 

In  all  advanced 
cases,  the  nutrition 
of  the  animal  is  in- 
terfered with  and, 
sooner  or  later,  the 
"tuberculous  cach- 
exia" appears.  It 
is,  however,  in 
many  cases  remark- 
able to  note  the  ex- 
tent of  lesions  in 
animals  that  are 
well  nourished  and 


Fig.  34.  Dorsal  aspect  of  bovine  lungs  sho'cving 
position  of  the  posterior  mediastinal  glands  ; 
[a,  h,  c,  c')  caudal,  ventral,  cephalic  lobes,  (/) 
esophagus,  (g)  muscular  pillars  of  diaphragm. 
(h)  posterior  aorta,  (i)  caudal  margin  of  the 
ligamentof  the  lung.  A.  Left  bronchial  gland. 
Mediastinal  glands  are  shown,  most  of  them 
resting  on  the  esophagus.  The  large  caudal 
gland  resting  on  the  pillars  of  the  diaphragm 
is  most  frequently  diseased  and  often  attains 
ail  enormous  size.  The  remaining  medias- 
tinal glands  are  arranged  in  tioo  sets  on  the 
right  and  left  margins  of  the  esophagus 
(Smith). 


ime  condition   by  the 


present  no  external 

signs  of  disease.      Animals  killed   in   pni 

butcher  are  sometimes  found  to  contain  extensive  and  widely 

distributed  lesions  of  tuberculosis.     In   general   tuberculosis, 


I88  TUBERCULOSIS 

many  of  the  symptoms  described  above  may  occur  simultane- 
ously. The  symptoms  of  acute  miliary  tuberculosis,  "gal- 
loping consumption,"  are  rapid  loss  of  flesh,  depression,  poor 
appetite,  cough,  weakness,  rapid  breathing,  harsh  respiratory 
sounds,  some  elevation  in  temperature,  increased  pulse  rate 
and,  sometimes,  enlarged  lymphatic  glands.  The  course  of 
this  form  of  tuberculosis  is  always  rapid  and  terminates  in 
death.  Acute  miliary  tuberculosis  occurs  when  large  num- 
bers of  tubercle  bacteria  are  discharged  into  the  blood  or 
lymph  currents.  They  are  then  carried  to  other  parts  of  the 
body,  filtered  out  in  the  capillaries  of  the  lungs,  liver,  spleen, 
kidneys  and  elsewhere,  causing  tubercular  lesions  in  each  of 
these  localities.  The  lesion  from  which  the  infectious  material 
entered  the  circulation  may  have  been  a  comparatively  small 
nodule.  This  form  of  the  disease  is  more  likely  to  appear  in 
young  animals  than  in  adults,  and  is  more  common  among 
swine  than  in  cattle. 

^  143.  Morbid  anatomy.  The  usual  direct  anatomical 
changes  following  the  invasion  of  tubercle  bacteria  are  the  for- 
mation of  nodules  or  tubercles.  A  tubercle  has  been  defined 
as,  "a  small  nonvascular  nodule  composed  of  cells  varying  in 
form  and  size  with  some  basement  substance  between  them 
and  with  an  inherent  tendency  to  undergo  central  necrosis." 
In  a  large  number  of  cases  the  individual  tubercles  are  dis- 
tinct and  easily  recognizable,  while  in  others  they  are  coal- 
esced, forming  a  mass  of  necrotic  tissue.  The  lesions  vary, 
therefore,  from  well  isolated  minute  or  larger  nodules  to 
masses  or  cavities  containing  a  purulent,  caseous,  or  calcified 
substance. 

The  location  of  the  primary  lesion  depends  upon  the 
channel  of  infection.  If  the  specific  organisms  are  lodged  in 
the  oral  cavity  or  pharynx  they  may,  through  an  accidental 
abrasion  of  the  mucosa,  be  taken  to  some  of  the  lymphatic 
glands  about  the  head;  if  they  are  taken  directly  through  the 
respiratory  passages  into  the  lungs  they  either  develop  no- 
dules in  the  lung  tissue  proper,  or  they    are  carried   through 


MORBID    ANATOIMY 


189 


the  lymphatic  system  to  the  lymph  gjlands  draining  the  lungs 
where  the  lesions  first  appear.  If  the  specific  bacteria  are 
first  lodged  in  the  intestinal  mucosa,  primary  tuberculous  ulcers 
may  develop  or  they  may  pass  into  the  mesenteric  lymphatics 
or  the  portal  vein.  It  may  happen  that  the  bacteria  may  be 
carried  by  means  of  the  lymph  or  blood  stream  and  lodged  in 
any  part  of  the  body,  such  as  the  brain,  kidneys,  spleen, 
testes,  ovaries,  bones,  joints,  and  subcutaneous  and  intermus- 
cular glands  and  serous  membranes.     The  evidence   at  hand, 


Fig.  35.      A  draiviuo-  of  a  section  ofveryyoniiix  tubercles  in  spleen  (  T/io>na). 

however,  seems  to  show  that  in  a  large  majority  of  ca.ses  the 
primary  lesions  are  located  in  one  of  the  five  following  organs  : 
(i)  in  the  lungs  or  the  lymphatic  glands  draining  them,  (2) 
in  the  lymphatic  glands  about  the  head,  (3)  in  the  mesenteric 
glands  and  intestines,  (4)  in  the  portal  glands  or  liver  sub- 
stance itself,  and  (5)  in  the  generative  organs  and  udder. 

It  not  infrequently  happens  that  the  apparent  primary 
lesions  occur  on  the  pleura,  peritoneum,  meninges  or  synovial 
membranes  while  the  organs  remain  free  from  disease.  In 
such  cases  the  lesions  consist  of  many   tubercles  varying  from 


I  go 


TUBERCULOSIS 


Fig.  36.     Section  of  a  tuberculous   heart  of  a   cow.     {a)    tuberculous   deposit 
surrounding  tlie  Iieart  muscle  and  base  of  the  larger  blood  vessels. 


:\[ORBID    ANATOMY  IQI 

one  to  ten  or  more  millimeters  in  diameter  or  ot  bunches  of 
closely  set  tubercles  which  are  more  or  less  flattened  or  irregu- 
lar in  shape,  owing  to  their  mutual  pressure.  Sometimes 
these  tubercles  are  attached  to  the  serous  membrane  by  a  small, 
tough,  fibrous  pedicle  ;  frequently,  however,  this  is  absent 
and  the  nodules  rest  bodily  upon  the  membrane. 

The  striuture  of  the  tubercle  consists  in  the  beginning  of  a 
few  cells  surrounding  the  invading  specific  organisms.  These 
are  soon  encased  by  a  zone  of  epithelioid  cells  and  giant  cells 
which  is  soon  surrounded  by  an  outer  layer  of  round  or 
lymphoid  cells.  The  central  portion  becomes  necrosed  and  as 
the  nodule  enlarges  the  central  necrotic  portion  becomes  cor- 
respondingly large. 

This  histological  structure  of  the  tubercle  is  typically  illus- 
trated in  the  beginning  avian  tubercle.  In  cattle  there  is  a 
strong  tendency  for  the  necrotic  tissue  to  become  infiltrated 
with  hme  salts  and  encapsulated.  In  certain  species  a  deposit 
of  fibrous  tissue  in  the  out,er  zone  of  the  tubercle  has  been 
observed.  In  the  smaller  and  more  susceptible  experimental 
animals  such  as  the  guinea  pig  and  rabbit  and  frequently  in 
swine,  the  lesions  are  of  a  more  diffuse  nature  infiltrating  the 
interstitial  tissue  with  the  tuberculous  mass  and  gradually 
encroaching  upon  the  parenchyma.  Circumscribed  tubercles 
may  also  be  present. 

In  secondary  or  generalized  tuberculosis  one  or  more  of 
the  organs,  such  as  the  omentum,  serous  membranes,  or  lym- 
phatic system,  may  become  more  or  less  thickly  sprinkled  witK 
minute  grayish  nodules  about  the  size  of  a  millet  seed.  These 
tubercles  are  at  first  almost  the  color  of  mother-of-pearl  but 
later  as  the  central  caseous  degeneration  begins  they  become 
grayish.     Giant  cells  are  usually  numerous. 

In  studying  the  lesions  in  a  fatal  case  of  tuberculosis  one 
may  find  with  varying  modifications  one  or  more  of  the  follow- 
ing conditions  : 

I .  The  primary  lesion  may  be  found  in  any  one  of  the 
organs  or  membranes.  Its  comparative  age  is  determined  by 
the  character  of  the  anatomical  changes.     It  may   be  entirely 


192  TUBERCULOSIS 

encysted,  caseous  or  calcareous  and  dead.  In  addition  to  the 
primary  focus,  there  may  be  a  succession  of  tubercles  of  vari- 
ous ages  distributed  in  one  or  more  organs. 

2.     The  lesions  may   be  restricted   to  one  organ,  as  the 

liver,  in  which  the  primary  focus  has  spread  by  continuity  due 

to  its  infiltrating  nature  until  the  destruction   of  the  tissues  ot 

the  organ  has  become  so  extensive  that  death  results.     Such 

cases  do  not  seem  to  be  common. 

3.  The  primary  lesion  may  be 
well  marked  and  accompanied  by 
miliary  tubercles  sprinkled  ex- 
tensively throughout  the  organs 
and  tissues  of  the  entire  body. 

4.  The  lesions  throughout 
the  body  may  resemble  each  other 
very  closely,  so  that  difficulty 
may  be  experienced  in  determin- 
ing the  primary  focus. 

In  the  lungs,  two  distinct 
forms  of  lesions  are  observed,  (i) 
The  air  cells  may  be  infiltrated 
with  the  tuberculous  mass  spread- 
ing directly  from  the  primary 
focus.  This  may  be  purulent, 
caseous  or  calcareous.  The  color 
may  be  whiti.sh,  gray  or  of  a  yel- 
lowish tinge.  (2)  The  lesions 
may  consist  of  miliary  tubercles. 
In  later  stages  these  nodules, 
more  or  less  translucent,  may  be- 
come yellowish,  caseated  and 
Fig.  37.     Tubcrcui  ,^  :u      calcareous  in  their  centers.   Large 


lung  showing  areas  oJ\  {a)  casea- 


tubercular  nodules  are  frequently 


Hon,    (b)  calcification,  and   [c) 
liquefaction.  formed  by  the  massing  of  several 

of  these  minute  tubercles. 
When  the  lungs  are  primarily  attacked  the  caudal  (prin- 
cipal)  lobes  are  most  frequently  involved.     Smith  considers 


""VH^H 

*   >    ' 

i^B 

\  J^^^^l 

.'':■                      '''/^-       ^ 

1 

-'                           * 

'^M 

^^  jBH    m- 

^H 

WH    V 

m 

L  . 

J| 

Fig. 


38.     Pliotoi!:raph  of  a  scciion  from  anterior  lobe  of  a  tuberculous  lung 
C07U,  sliowino-  tuberculous  infiltration  and  calcified  areas. 


194 


TUBERCULO.SIS 


the  seemiug  predilection  for  the  larger  lobes  to  be  due  to 
mechanical  conditions.  The  writer  has  found,  however,  that 
in  certain  herds  that  have  been  killed  after  the  tuberculin  test, 
thejprimary  and  only  lung  lesions  were  in  the  ventral  and 
cephalic  lobes.  It  is  important  to  note  that  usually  the  bron- 
chial glands  are  also  involved.  When  the  pleurae  are  affected 
the  lesions  consist  of  nodules  varying  in  size  from  that  of  a 
millet  seed  to  a  large  pea,  sprinkled  more  or  less  thickly  on 
one  or  both  of  the  visceral  or  parietal   surfaces.     These  form 


Fig.  39.     Plwloi::iapli  of  pleura  slnncin<i  small  tuberculous  nodules. 


the  "pearl  disease"  Pcrlsucht  of  the  German  and  the 
"grape  disease"  of  the  English  writers.  If  they  become 
confluent,  large  masses  are  found. 

Tuberculosis  of  the  thoracic  glands  is  very  common  and 
usually  accompanies  lesions  in  the  lungs;  but  the  lungs  may 
be  healthy  and  the  glands  involved.  (See  figures  for  location 
of  glands.)  The  primary  lesions  may  be  and  often  are  found 
in  the  lymphatic  glands  about  the  head. 


MORBID    ANATOMY 


195 


In  the  abdominal  cavity  the  organs  most  frequently  in- 
volved are  the  peritoneum,  mesenteric  lymph  glands,  portal 
lymph  glands  and  liver.  The  kidneys,  spleen,  ovaries  and 
uterus  are  more  rarelj^  the  seat  of  tuberculous  tumors.  Ulcers 
in  the  intestine  have  not  been  common  in  the  writer's  observa- 
tion.    The  ulcers  in  the   cases   observed    have    been    isolated 


Irv 


:^-v^. 


^  *  '  *\  ;  %  £^  ^  .,.-"^ 


'/'*^:^i6:-r     -'i-'.>\r: 


i^4' '- 


^,f 


'£, 


% 

Fig.  40.      Tubercles  on  the  mesentery  of  a  eorc  {Harding). 


with  elevated  borders  and  a  depressed  center.  Sections  show 
that  the  tuberculous  infiltration  extends  outward  and  to  a  cer- 
tain extent  undermines  the  mucosa.  Tuberculosis  of  the  testis 
is  sometimes  found.  The  udder  becomes  the  seat  of  tuber- 
culous   deposits    in    a    small    percentage    of    cases.       It     is 


IQD  TUBERCULOSIS 

more    often    affected    in    cases    of    generalized    tuberculosis. 

When  the  primary  infection  is  restricted  to  a  single   focus 

the  disease  is  said  to  be  localized.     When  the  specific  bacteria 


41.     A  photograph  of  the   tuberculous   nodules  on  the  o>ntntum 
from  an  advanced  case  of  generalized  tuberculosis. 


are  spread  from  the  primary'  lesions  through  the  agency  of  the 
Ijnnph  and  blood  streams,  sprinkling  other  organs  with  the 
infecting  bacteria,  each  of  which    becomes    the   starting  point 


MORHID    ANATOMY 


197 


for  the  development  of  a  new  tubercle,  the  disease  has  become 
generalized. -■■ 

It  was  formerly  considered  that  when  the  lesions  existed 
in  both  of  the  large  (abdominal  and  thoracic)  cavities  of  the 
body  the  disease  was  generalized.  It  is  possible,  however, 
for  it  to  be  generalized  when  the  lesions  are  restricted  to  the 
orcrans  of  one  cavity,  as  the  secondary  seeding  with   the  bac- 


FiG.  42.     A  p/iofooraph  of  several  inbercHlous  ulcers  in  the  inlesline 
■    of  a  CO  70. 

teria  that  have  escaped  from  a  primary  focus  through  the  cir- 
culation may  be  restricted  to  the  cavity  in  which  the  first 
lesion  developed.  It  seems  better,  therefore,  to  accept 
Ostertag's  views  and  classify  local  and  generalized  tuberculosis 

*The^ederal  meat  inspection  regulations  state  that  animals  affected 
with  -extensive  or  generalized  tuberculosis  "  are  to  be  condemned. 


TUBERCULOSIS    IN    SWINE 


in  accordance  with  the  nature  of  the  lesions  rather  than  their 
distribution  in  the  body. 

The  fact  is  worthy  of  consideration,  that  very  often  cattle 
killed  after  reacting  to  tuberculin  do  not  show  extensive  dis- 


FiG.  43.     A  photoi^raph  of  a  section  of  a  tuberculous  ulcer,  from  a 
corv's  intestine,  sho7c'in<rinfltration  under  the  tnaroinal  mucosa. 

tribution  of  lesions.  Frequently  animals  are  killed  soon  after 
infection  has  taken  place,  in  which  case  the  lesions  are  re- 
stricted to  a  single  lymphatic  gland  or  other  organs.  In  other 
cases  old  lesions  of  considerable  proportion  are  found  as  shown 
in  Fig.  36,  where  the  heart  muscle  is  entirely  encased  in  a 
thick  calcareous  tuberculous  deposit.  In  this  case,  the  animal 
was  in  good  fle.sh  and  killed  for  beef  without  a  suspicion  that 
it  was  in  any  way  diseased. 


TUBERCULOvSIS  IN  vSWINE 

§  144.  Channels  of  infection.  It  is  stated  that  among 
swine  young  animals  belonging  to  the  precocious  breeds  seem 
to  be  more  liable  to  tuberculosis  than  others.  In  nine  eases 
out  of  ten  the  animals  are  infected  by  ingestion.  The  pig 
easily  becomes  tuberculous  when  fed  on  material  rich  in  tuber- 
cle bacteria.  If  pigs  are  fed  on  the  refuse  from  dairies  and 
cheese  manufactories  in  districts  where  there  is  much  tubercu- 


SYMPTOMS  199 

losis  in  cattle  or  on  tuberculous  viscera  they  readily  become 
infected.  Mohler  found  that  when  hogs  were  fed  on  tubercu- 
lous milk  for  three  days,  and  killed  and  examined  post-mortem 
107  days  later  that  83.3  per  cent  were  tuberculous.  Hogs  that 
received  infected  milk  for  30  days  and  were  allowed  to  live  fifty 
days  thereafter  100  per  cent  were  affected.  Infection  through 
the  respiratory  tract,  while  it  is  certainly  possible,  seems  to  be 
rare.  The  piggeries  where  the  refuse  from  butter  and  cheese 
factories  is  fed  and  those  which  join  abattoirs  supply  the  ma- 
jority of  swine  found  on  post-mortem  to  be  tuberculous. 

Ostertag  has  called  special  attention  to  this  disease  as 
existing  among  swine  in  certain  parts  of  northern  Denmark 
and  Germany,  where  there  was  much  tuberculosis  in  cattle^ 
and  where  the  swine  were  fed  the  slime  from  creamery  separa- 
tors. Experiments  show  the  possibility  of  infection  by  means 
of  the  sputvim  of  tuberculous  people. 

In  the  cases  which  have  come  to  notice  there  is  ver}^ 
strong  evidence  that  the  swine  were  infected  by  being  fed  the 
milk  from  tuberculous  cows.  In  one  of  these  cases,  the  tuber- 
culin test  showed  that  a  large  number  of  the  cows  from  which 
the  milk  was  obtained  were  affected. 

v?  145.  Symptoms.  In  most  cases  tuberculosis  of  the 
pig  is  first  recognized  at  the  abattoir.  Sometimes,  however,  it 
causes  local  and  general  troubles,  which  varj'  according  to  the 
organ  or  system  attacked.  The  following  symptoms  have 
been  noted. 

Its  localization  in  the  abdominal  organs  causes  the  arrest 
of  fattening  and  the  progressive  wasting  of  the  subject.  The 
mucous  membranes  become  pale,  the  hide  becomes  dirty  and 
there  is  usually  either  constipation  or  diarrhea.  The  animal 
is  in  low  spirits,  the  corkscrew  of  its  tail  is  straightened,  the 
abdomen  is  pendulous  and  the  eyes  are  sunken.  Palpation  of 
the  abdomen  is  painful  and  may  reveal  more  or  less  volumi- 
nous masses,  due  to  the  changes  in  the  mesenteric  glands.  It 
is  common  to  find  glandular  tumors  in  the  submaxillary 
region  or  at  the  thoracic  inlet.      In  this  form,  the  malady  may 


200  TUBERCULOSIS    IX    SWINE 

last  several  months,  but  death  supervenes  rapidly  if  the  lesions 
become  generalized  by  the  scattering  of  the  bacteria  through 
the  blood  stream.  Primary  pulmonary  tuberculosis  is  very 
rare  but  sooner  or  later  lung  lesions  complicate  abdominal 
tuberculosis.  They  betray  themselves  at  the  outset  by  a  short, 
dry,  abortive  cough  and  by  difficult  respiration.  The  cough 
soon  becomes  paroxysmal  and  painful  and  is  often  followed  by 
vomiting  ;  the  respiration  becomes  hurried  and  gradually  pain- 
ful and  more  difficult,  wasting  is  very  rapid,  and  death  super- 
venes in  a  few  weeks. 

The  scrofula  of  swine  (glandular  tuberculosis)  usually 
shows  itself  by  a  puffing  up  of  the  face,  which  a  careful  exam- 
ination shows  to  be  lifted  up  by  the  subjacent  glands,  these 
being  enlarged,  indurated,  still  fairly  mobile  and  free  from 
heat  or  tenderness.  The  retropharyngeal,  superior  cervical 
and  sublingual  glands  are  usually  affected,  forming  a  kind  of 
necklace  of  unequal  and  knotty  tumors,  reaching  from  ear  to 
ear  and  becoming  larger  under  the  neck  between  the  rami  of 
the  lower  jaw.  Similar  tumors  may  be  developed  at  the 
thoracic  inlet,  behind  the  shoulder  or  in  the  groin,  which,  as 
they  increase  in  size,  become  harder  and  more  adherent  to  the 
neighboring  tissues.  Sometimes,  however,  a  slight  fluctua- 
tion is  perceptible.  The  tumor  may  suppurate  and  discharge 
a  small  quantity  of  a  thick  and  gruraous  pus,  but  the  glandu- 
lar tumor  does  not  disappear  and  the  opening  into  the  abscess 
remains  for  a  long  time  as  a  fi.stula. 

There  may  be  swellings  of  the  bones,  causing  a  true 
tuberculous  arthritis  when  the  lesions  happen  to  be  situated 
at  the  level  of  an  epiphysis.  Persistent  lameness,  fistulous 
wounds  suppurating  indefinitely,  necrosis  and  caries,  are  the 
complications  of  the  lesions  of  the  bone,  the  development  of 
which  is  always  extremely  slow. 

§  146.  Morbid  anatomy.  The  manifestations  of  tu- 
berculosis in  swine  are  exceedingly  interesting.  Nocard 
found  the  lesions  to  consist  of  miliary  granulations  which 
rapidly  become  caseous,   as  in  cattle,  but  which  more  rarely 


Plate  I. 


TUBERCULOUS     LUNGS     OF     HOU 


MORBID    ANATOMY 


contain  calcareous  salts.  General- 
ization is  common,  in  which  case 
the  viscera  are  thickly  sprinkled 
with  gray  granulations  which  are 
translucent  throughout,  or  opaque 
in  their  centers,  and  quite  analo- 
gous to  those  found  in  tubercular 
lesions  in  other  animals. 

As  the  disease  most  often  re- 
sults from  ingestion  of  the  virus, 
the  digestive  apparatus  and  the  cor- 
responding lymphatic  glands  (sub- 
maxillary, parotid,  pharyngeal,  su- 
perior cervical,  mesenteric,  sub- 
lumbar,  etc.)  may  be  decidedly 
diseased,  while  the  other  organs  re- 
main practically  intact.  Lesions  of 
the  small  intestine  and  of  the 
cecum  are  common  and  take  the 
form  of  ulcers  of  the  mucous  mem- 
brane, of  miliary  nodules  or  of 
tuberculous  infiltrations,  involving 
at  once  the  mucous,  the  muscular, 
and  subserous  tissues.  The  lesions 
in  the  liver  take  the  form  either  of 
miliar\'  granulations,  which  are 
yellow  and  caseous  and  scattered  in 
great  numbers  through  the  thick- 
ness of  the  organ,  or  else  of  rounded 
nodules  which  are  yellowish  white 
in  color,  varying  in  size  from  that 
of  a  pea  to  a  hazel  nut  and  of  a 
tough  consistency.  On  section 
they  appear  sometimes  to  be  firm, 
homogeneous  and  fibrous  ;  some- 
times .softened  in  the  center, 
often  infiltrated  with  calcareous 
salts.      The    peritoneum    and     the 


Fig.  44. 


Tiibitculous  spleen- 


irotit  a  pii:  . 


202  TUBERCULOSIS    IN    SWINE 

pleura  are  sometimes  the  seat  of  an  eruption  of  fine  granula- 
tions which  remain  in  a  state  of  miliary  nodules.  Lesions  like 
those  in  the  liver  may  exist  in  the  lungs,  but  generally  there 
is  found  in  these  organs  an  innumerable  number  of  minute, 
translucent,  gray  granulations,  caused  by  the  dissemination  of 
tubercle  bacteria  through  the  blood  stream,  in  which  case  the 
liver,  the  spleen,  the  kidneys,  the  medulla  of  the  bones,  and 
the  mammae  may  be  infiltrated  with  similar  growths. 

Mohler  has  reported  the  results  of  the  examination  of 
120,000  infected  hogs  of  which  93.3  per  cent  had  tuberculous 
glands. 

It  is  common  to  find  lesions  localized  in  one  or  several 
lymphatic  glands.  The  pharyngeal  and  submaxillary  glands 
are  the  ones  most  often  affected.  They  become  voluminous, 
hard  and  knotty,  as  they  have  undergone  a  true  fibrous  trans- 
formation and,  consequently,  are  difficult  to  cut.  This  is 
shown  by  the  creaky  sound  under  the  cutting  instrument.  In 
section  they  have  the  appearance  of  old  fibrous  tissues;  here  and 
there  small  yellow  foci  are  seen  of  a  softer  consistency,  almost 
caseous;  sometimes  veritable  purulent  collections  are  found, 
either  encysted  or  in  communication  with  the  exterior.  If 
one  submits  the  caseous  or  purulent  matter  to  a  bacteriological 
examination,  tubercle  bacilli  are  not  usually  found.  The  bac- 
terium, however,  is  present  and  if  this  matter  is  inoculated 
into  the  peritoneal  cavity  or  the  subcutaneous  tissue  of  guinea 
pigs  it  will  produce  tuberculosis. 

These  chronic  glandular  lesions,  with  their  very  slow  pro- 
gress, have  long  been  looked  upon  as  constituting  the  scrofula 
of  swine,  and  to  scrofula  was  also  assigned  the  tuberculous 
lesions  of  bones  (ribs,  vertebrae,  articulations,  shoulder  blades, 
hip  bones)  which  are  common  in  pigs,  both  young  and  old. 

The  older  authors  noted  that  the  ancient  scrofula  was 
often  accompanied  by  visceral  tuberculosis,  but  they  refused  to- 
admit  the  identity  and  even  the  relationship  of  the  two  af- 
fections. 

The  generalization  of  the  disease,  especially  in  the  mus- 
cular tissue,  is  reported  by  several  ob.servers.     Moule  called  at- 


TUBERCULOSIS    IX    OTHER    MAMMALS  203 

tention  to  this  peculiarity  of  the  disease.  Stockman  shows 
that  while  the  disease  is  ordinarily  generalized,  muscular 
lesions  may  exist  in  swine  in  the  absence  of  generalization. 
Zschokke  has  called  special  attention  to  the  localization  of 
tuberculous  lesions  in  the  head  of  swine,  especially  in  the  nares 
and  brain. 


TUBERCULOSIS  IX  OTHER  MAMMALS 

^  147.  Genera  affected.  It  is  stated  that  all  species 
are  sometimes  attacked.  Tuberculosis  in  the  horse  is  rare, 
although  a  total  of  many  cases  have  been  reported.  Bang  has 
collected  twenty-nine  cases.  In  Saxony  .oS  per  cent  of  the 
horses  (3,500)  that  were  slaughtered  were  tuberculous.  In 
this  and  most  countries  there  are  no  reliable  statistics  respect- 
ing the  extent  of  the  disease  in  this  species.  M'Fadyean  has 
pointed  out  the  fact  that  in  a  considerable  number  of  cases  of 
equine  tuberculosis,  where  the  horses  have  been  fed  milk  from 
tuberculous  cows,  the  morbid  anatomy  differs  but  slightly  from 
that  in  tuberculous  cattle.  Recently  several  authors  have 
reported  isolated  cases  in  Europe.  In  this  country  horses  are 
practically  free  from  it. 

Sheep  and  other  domestic  animals  are  reported  to  suffer 
more  or  less  extensively  from  this  disease.  All  of  the  so-called 
tuberculosis  in  sheep  that  I  have  examined  proved  not  to  be 
tuberculosis  but  the  "  nodular  disease  "  caused  by  an  animal 
parasite,  {Oesopagostoiiia  Cohimbianu))i) .  A  few  cases,  how- 
ever, have  been  reported. 

Tuberculosis  in  dogs  and  cats  is  quite  rare  but  several 
cases  in  each  genus  are  on  record. 


AVIAN  TUBERCIXOSIS 

§148.  History.  In  America,  tuberculosis  in  fowls  was  de- 
scribed by  Pernot  in  Oregon  in  1900.  In  1903  Moore  and  Ward 
found  the  disease  in  California,   where  in  certain  flocks  it  was 


204  AVIAN    TUBERCULOSIS 

very  destructive.  It  was  recognized  by  the  owners  as  "  spotted 
liver,"  going  light,  and  rheumatism.  In  1900  it  was  described 
by    Burnett    from    northern    New    York.     In    Europe    it  has 

been  known  for  a  long  time. 
.- rrr'^-'T^.i-  i;   149.     Symptoms.      The 

V    '•  .^  •-•  symptoms  described   as   quite 

/  '»**",  constant  are  emaciation,  which 

*<  in    advanced    cases    becomes 

/^       '  extreme,    and    anemia.     The 

J   s  *    I       -  comb,  the  skin,  and  the  visi- 

•i"^^,  hie    mucosa    about    the    head 

\  '«'  •  y  are    usually    pale.       As     the 

;  course  of  the  di.sease  advances 

/  ^  the    feathers    become    ruffled 

and  the  fowls  are  weak,  dump- 
ish and  move  about  very  little. 
The  eyes  are  bright  in  most 
cases  until  the  end  is  near. 
'    .  The  appetite  is  good,  and  the 

^'  'X 

V    ,       •         /  temperature  is  in   most  cases 

•  '  >-v  .  '^     ""     ' 

.1  '^  ~f     '^.    ^    ^N    rarely   it  is  subnormal.     The 

/I     ^    ,     ,'         V,,  blood    is    pale.     The    hemo- 

(    '    /^'•        I     /  "        '      globin  varies  from  thirty-five 

*     \     ■•  .      N  to  seventy  per  cent   as  tested 

•  '  with    Gowers'     hemoglobino- 

meter.  The  red  blood  corpus- 
cles var}-  from  1,010,000  to 
Fig.  45-  Avian  tubercle  bacteria.  2,600,000  per  cubic  milli- 
(/ )  from  /tver  tissue  of  a  fowl,  {2)  meter.  There  appears  to  be  a 
a  p/wtograph  from  a  preparation  slight  increase  in  the  number 
from  a  glycerine  agar  culture,     x       of  white  corpuscles,  especially 

about    600.  r  ^^  ■  1-1 

of  the  eosinophiles. 
Tuberculous  fowls  are  often  lame.      Pernot  mentions  this 
as  one  of  the  important   symptoms  in   the  cases  he  observed. 


w      V     '        -^      \.^^  fowls    eat    ravenously   until  a 

"Vi""  .     -^^     ^-    ,f^  few  days  before  death.     The 

""si     within     the     normal      limits, 


AVIAN    TrUERCLE    15ACTERIA 


'■^5 


It  is  due  to  joint  lesions  in  some  cases.      In  others  it  appears 

to  be    due   to   extensive    lesions    in    the 

viscera. 


i^^  150.  The  avian  tubercle  bac- 
teria. These  organisms  resemble  quite 
closely  those  of  the  human  and  bovine 
varieties  in  their  size  and  general  mor- 
phology as  they  are  found  in  the  tissues 
of  the  fowl.  A  measurement  of  over  two 
hundred  individual  organisms  in  cover 
glass  preparations  made  directly  from 
organs  of  fowls  gave  the  following  :  In 
the  liver  the  length  varied  from  1.2  to 
3.5  /<,  in  the  spleen  and  in  the  skin  they 
varied  from  i  to  4  /(  in  length.  A  gen- 
eral average  gave  a  length  of  2.7  /<.  They 
often  appear  in  these  preparations  in 
dense  masses.  Chains  made  up  of  a 
number  of  short  elements  are  rarely  pres- 
ent. Granules  are  occasionally  observed. 
In  the  preparations  from  the  skin  a  con- 
.siderable  number  of  them  contain  polar 
granules  and  not  infrequently  three  such 
bodies  were  noticed  in  a  single  individual. 
Perhaps  the  most  striking  feature  con- 
cerning these  organisms  in  the  tissues  is 
their  enofmousj  numbers.  Sibley  has 
called  attention  to  the  similarity  of  avian 
tubercle  bacteria  [to  those  of  leprosy  in 
that  thej^  nitiltiply  to  such  enormous 
numbers  without  a  pronounced  breaking 
down  of  the  tissues. 

This  variety  is  more  easily  obtained 
in  pure  culture  from  the  lesions  than  the 
human  or  bovine  forms.  Mooreobtained 
pure   cultures    in   about   20  per  cent   of 


Fig.  46.  ^  g/j'ii'rine 
ag^iir  culture  of  avian 
tubercle  bacteria.  Cul- 
ture four  Tl'CcA'S  old. 


206  AVIAN    TUBERCULOSIS 

serum  tubes  inoculated  directly  from  tuberculous  lesions  in 
fowls.  It  grows  readily  on  glycerin  agar,  Dorset's  egg 
medium,  potato  and  in  glycerin  bouillon. 

The  colonies  on  glycerin  agar  vary  from  one  to  three 
millimeters  in  diameter.  The  central  portion  is  raised  and  of 
a  slightly  yellowish  tint  as  observed  under  a  hand  lens.  This 
central  part  is  surrounded  by  a  flat  expansion,  about  two- thirds 
the  thickness  of  the  center,  varying  from  one-half  to  one  milli- 
meter in  width,  with  ray-like  projections  radiating  from  it  and 
extending  into  the  outer  and  very  thin  band  of  growth  with  a 
lobulated  margin.  On  the  egg  medium  of  Dorset  the  growth 
is  not  more  vigorous  than  that  upon  glycerin  agar.  Potato 
cultures  are  quite  vigorous,  wrinkled  and  of  a  yellowish- 
brown  color. 

Fowls  inoculated  in  the  abdominal  cavity  or  subcutane- 
ously  with  from  one-half  to  one  cubic  centimeter  of  a  glycerin 
bouillon  culture  develop  either  localized  or  generalized  tuber- 
culosis in  from  six  weeks  to  three  months,  but  a  much  longer 
time  is  necessary  to  destroy  them. 

Rabbits  and  guinea  pigs  are  not  readily  infected  by  the 
inoculation  of  pure  culture.  Moore  and  Ward  failed  to  pro- 
duce any  tuberculous  lesions  in  these  species. 

i^  151.  Morbid  anatomy.  The  lesions  are  widely  dis- 
tributed, and  vary  much  in  their  location  in  different  individ- 
uals. The  liver  is  most  frequently  involved.  The  spleen, 
intestines,  mesentery,  kidneys,  lungs  and  skin  are  affected  in 
order  mentioned.  The  appended  table  gives  the  distribution 
of  the  lesions  in  17  cases  observed  by  Moore. 


MORBID    ANATOMY 


207 


TABLE   SHOWING   THK,    DISTRIHUTION    OF    I.RSIONS    IN    Tl'HER- 
/  CULOUS   FOWLS. 


1      ^0^ 

C)KC,.\N 

r,    INVOI. 

VKI).* 

Skin 

1,^^! 

Liver 

Spleen 

Intes- 
tine 

Mesen- 
tery 

Kidney    Ovary  1 

Lungs 

Bones 

,k' 

XX 

1 

2     D 

1 

XXX 

^  K 

XXX 

._-  __ 

4  K    107 

5  K    105  2- 

6  K    107.4 

-7     K"       107   2 

XX 
XXX 
XXX 

"xx 

_ 
XX           X 



XX 

X 

X 

XXX 
X 

XXX 
X 

XX 

8  D 

X 
X 

9   I> 

XX 

108.4 

106.4 

107.4 

107 

107.6 

106.8 

XXX 
XXX 
XXX 
XXX 
XXX 
XXX 

X 

X 

XX 

11  K 

12  K 

13  K 

14  K 

15  K 

16  D 

X 
X 

i 

XXX 

XXX 

— - 

XX 

1 

. 

XXX 
XXX 

■ 

17  K 

I 

105 

1  XXX 

XX 

1 



*The  relative  numbers  of  tubercles  are  indicated  by  the  number  of  Xs.  XXX 
indicates  an  extensive  invasion,  XX  a  less  number  of  tubercles,  and  X  very  few. 
Figures  47  and  48  show  extent  of  lesions  represented  by  X.XX. 

The  tubercles,  especiall}'  in  the  liver,  in  the  earlier  stages 
of  the  disease,  are  small  greyish  points  varying  from  0.25  to 
i.o  millimeter  in  diameter.  In  advanced  cases  they  are  larger. 
They  have  a  cheesy  con.sistency,  and  are  easily  removed  from 


208 


AVIAN    TUBERCULOSIS 


the  surrounding  tissue.  The  removed,  necrotic  nodules  have 
a  roughened  surface.  The  color  is  greyish  or  whitish  in  the 
early  stages,  but  in  the  later  cues  it  changes  to  a  yellowish 
tint.     Occasionally  there  are  two  distinct  crops  of  tubercles, 

one  consisting  of  no- 
dules 4  to  6  milli- 
meters in  diameter 
and  separated  by  a 
centimeter  or  more, 
and  the  other  of  close- 
ly set  grayish  tuber- 
cles 0.25  to  0.5  mm. 
in  diameter.  In  some 
cases  the  tubercles 
are  few  in  number 
but  larger  i  n  size. 
The  liver  cells  be- 
tween the  tubercles 
are  usually  in  a  state 
of  more  or  less  degen- 
eration, and  frequent- 
ly fat  globules  are 
numerous.  The 
blood  spaces  are  more 
than  normally  dis- 
tended with  blood. 
The  lesions  in  the  spleen,  like  those  in  the  liver,  consist  of 
minute  or  larger  tubercles  of  a  grayish  or  of  a  yellowish  tint. 
The  central  portions  of  the  larger  tubercles  are  often  homo- 
geneous, darker  in  color  and  more  or  less  hyaline  in  appear- 
ance and  consistency. 

The  tubercular  growths  in  the  intestine  start  in  the  walls 
of  the  intestine.  They  present  a  glistening  appearance,  gray- 
ish in  color  and  firm  to  the  touch.  Frequently  they  are 
confluent.  When  single  they  vary  from  i  to  10  qim.  in  ' 
diameter.  They  are  usually  sessile  on  the  intestine  but  on 
the  mesentery  they  are  frequently  pedunculated,  varying  from 


Fig.  47.     A  p/io/ograph  of  a  tuberculous 
liver  from  a  foivl. 


MORBID    ANATOMY 


209 


2  to  5  mm.  in  length.  On  section  the  young  tubercles  exhibit 
a  grayish,  glistening  surface,  but  the  more  advanced  nodules 
contain  recognizable  necrotic  centers.  In  the  larger  tubercles 
on  the  intestines  the    necrotic    centers    frequently    open    into 

the  lumen. 

The  skin  lesions  consist  of  a  cellular  infiltration  usually 
about  the  root  of  the  feathers.       Frequently  the  nodules  be- 


FiG.  48.     A  photograpn  .,  .  ...:..^^        ■  ^^     ,rle /,'0,najbwl  s/wu',»g 
the  necrotic  center  and  surrounding  zones.     Enlarged. 

come  confluent.     They  may  or  may  not  involve  the  subcuta-' 
neous  connective  tissue. 

The  microscopic  examination  of  the  tubercles  of  the  liver 
shows  them  to  consist  of  a  necrotic  center  surrounded  by  an 
irregular  zone  of  epithelioid  and  giant  cells.  This  is  sur- 
rounded by  a  band  of  tissue  consisting  for  the  greater  part  of 
liver  cells  more  or  less  disintegrated,  free  nuclei  and  a  few 
infiltrated  round  cells.     This  zone  is  circumscribed  by  a  nar- 


AVIAN    TUBERCULOSIS 


row  reactionary  band  consisting  very  largely  of  round  cells. 
The  structure  is  constant  in  both  small  and  large  tubercles, 
and  not  strikingly  different  from  the  structure  of  tubercles  in 


Fig.  49.     A  photograph  of  a  tuberculous  mesentery  of  a  foTcl. 
are  a  few  small  tubercles  on  the  intestine. 


There 


certain  of  the  mammals.     The  larger  nodules  seem   in   some 
instances  to  be  the  result  of  a   contiuuous  growth  of  a  single 


)IFFEKKXTIAr,    DIACXOSIS 


211 


tubercle,  and  in  others  to  have  resulted  from  the  coalescence 
of  a  number  of  small  ones.  The  necrotic  center  and  reaction- 
ar\'  zone  of  round  cells  are  beautifully  demonstrated  by  their 
reaction  to  nuclear  stains. 

§   152.      Differential  diagnosis.     Tul)erculosis  in   cattle 


Fig.  50.     A  photoiiraph  of  the  head  and  part  of  the  neck  of  a 
tuberculous  fowl. 

and  swine  is  to  be  differentiated  from  actinomycosis,  glanders, 
and  various  parasitisms  resulting  in  nodules  largely  in  the 
walls  of  the  intestine.  In  cattle  the  nodules  are  produced  by 
an  Oesophagostoma.     In    sheep    the    nodules   are   caused  by 


212  AVIAN   TUBERCULOSIS 

O.  Coluvibianum  Curtice.  In  chickens  a  nodular  taeniasis  of 
the  intestine  is  not  infrequently  mistaken  for  tuberculosis. 
Abscesses  and  necrotic  foci  due  to  various  agencies  must  also 
be  distinguished  from  tuberculous  lesions.  Enlargement  of  the 
lymphatic  glands  may  be  due  to  Hodgkin's  disease. 

In  cases  of  actinomycosis,  the  ray  fungus  can  usually  be 
detected  on  a  microscopic  examination.  Bacteruun  mallei  can 
be  found  either  in  cultures  or  by  guinea  pig  inoculations  in 
cases  of  glanders,  and  in  parasitic  diseases  the  specific  animal 
parasite  can  be  found  if  diligently  sought.  A  careful  study  of 
the  recent  lesions,  especially  in  the  nodules  caused  by  the 
animal  parasites,  will  show  that  they  are  not  structurally  like 
the  tubercle  as  described  above. 

From  the  symptoms  and  morbid  anatomy  it  is  clear  that 
hard  and  fast  lines  for  diagnosing  tuberculosis  cannot  be  laid 
down.  As  a  rule  the  lesions  are  characteristic,  although  there 
are  many  exceptions.  In  making  a  positive  diagnosis  one 
must  rely  upon  the  discovery  microscopically  of  the  specific 
bacterium,  the  result  of  animal  inoculation  or  the  effect  of 
tuberculin. 

The  tubercle  bacteria  can  be  tound  by  making  and  prop- 
erly staining  cover-glass  preparations  from  the  tuberculous 
tissues  or  discharges  in  a  certain  number  of  cases.  When 
these  tuberculous  lesions  open  into  the  respiratory  tract  the 
specific  bacteria  can  almost  always  be  found  in  the  expectora- 
tion. This  is  especially  true  in  men,  and  Ravenel  and  others 
have  shown  that  it  is  often  true  in  cattle.  In  old  and  in  the 
very  recent  tuberculous  lesions,  it  is  not  so  easy  to  detect  these 
organisms  microscopically.  When  there  is  doubt  animal  inoc- 
ulation gives  quite  prompt  results. 

Tuberculosis  in  fowls  is  to  be  differentiated  from  certain 
other  affections,  such  as  lymphadenoma  and  sarcoma  of  the 
liver,  asthenia,  nodular  taeniasis  and  excessive  infestion  with 
the  air  sac  mite  {Cytodites  7itidiis).  Because  of  a  close  simi- 
larity in  the  general  symptoms,  and,  in  certain  cases,  of  the 
gross  lesions,  between  tuberculosis  and  certain  other  affections, 
the  findings  of  a  somewhat  careful  examination  are  necessary 


aSlTY  ) 

DIFFERENTIAL    DIAGNOSIS  2  1^ 

to  warrant  a  positive  diagnosis.  In  the  living  fowl  it  seems  as 
yet  to  be  impossible  to  fix  upon  any  diagnostic  symptoms. 
At  post-mortem,  however,  properly  stained  cover-glass  prepa- 
rations from  the  tubercles  will  reveal  the  presence  of  tubercle 
bacteria.  This  renders  the  positive  diagnosis  in  the  dead  fowl 
a  comparatively  easy  task. 

The  positive  diagnosis  of  tuberculosis  rests  in  : 

1.  Finding  the  tubercle  bacterium  on  a  microscopic 
examination  of  the  lesions. 

2.  The  production  of  tuberculosis  in  experimental  ani- 
mals by  inoculating  them  with  the  suspected  tuberculous 
material. 

3.  Obtaining  a  typical  reaction  after  the  injection  of 
tuberculin. 

§  153.  Microscopic  examinations.  The  diagnosis  by 
microscopic  examinations  is  possible  when  one  has  the  dis- 
charge from  a  lesion,  such  as  the  sputum  when  the  lungs  are 
involved.  In  case  of  tubercular  abscesses,  the  examinations 
should  be  made  from  the  scrapings  of  the  walls  of  the  abscess 
rather  than  from  the  purulent  contents.  It  is  often  possible 
to  find  tubercle  bacteria  in  sections  of  the  diseased  organs. 

A  viethod  for  staining  tiiberrlf  hacteria.  Stain  the  cover-glass  with 
fresh  carbol  fuchsiii.  Place  a  few  drops  of  the  stain  on  the  film  side  of 
the  cover-glass  preparation  and  hold  it  over  a  flame  with  forceps  nntil 
steam  is  given  off.  Allow  the  hot  stain  to  act  for  from  3  to  5  minutes, 
or  the  preparation  may  be  floated  on  the  carbol  fuchsin  in  a  watch  glass 
without  heat.  In  this  case  it  is  allowed  to  act  for  from  10  to  15  minutes. 
The  preparation  is  then  rinsed  in  water  and  decolorized  by  treating  it 
with  a  10%  solution  of  nitric  or  sulphuric  acid  for  from  V  to  i  minute. 
It  is  again  rinsed  in  water,  when  it  is  ready  for  examination.  It  can  be 
dried  and  mounted  permanently  in  balsam.  The  tubercle  bacteria 
should  be  stained  a  deep  reddish  color.  All  other  bacteria  or  animal 
tissue  in  the  preparation  should  be  nearly  or  quite  decolorized.  If 
desired,  a  counter-stain,  such  as  alkaline  methylene  blue,  may  be  used 
after  decolorizing ;  that  is,  the  preparation  should  be  again  stained  for 
about  I  minute  in  alkaline  methylene  blue,  rinsed  in  water,  and 
examined  as  before.  In  these  preparations  the  tubercle  bacteria  are  red 
and  the  other  organiams  and  cells  are  blue.  A  counter-stain  is  of  little 
value  in  preparations  made   for   simple    diagnostic    purposes.      When    a 


214  TUBERCULOSIS 

counter-stain  is    desired   Gabbett's   decolorizing   and    counter-staining 
solution  is  very  convenient. 

gabbett's   solution 

Methylene    blue    (powder) 2  grams 

10%  sulphuric  acid 100  cc. 

After  staining  with  the  carbol  fuchsin  treat  the  preparations  with 
this  mixture  until  the  film  has  a  faintly  bluish  tint.  This  solution 
decolorizes  and  counter-stains  at  the  same  time.  Care  must  be  taken 
not  to  confuse  the  other  acid  fast  bacteria  with  those  of  tuberculosis. 
The  acid  fast  bacteria  other  than  tubercle,  are  decolorized  with  acidulated 
alcohol  (3  per  cent  hydrochloric  acid  in  95  per  cent  alcohol). 

§  154.  Animal  inoculation  for  purposes  of  diagnosis. 
Guinea  pigs  are  preferable,  although  rabbits  may  be  used. 
With  tuberculous  tissue  either  of  the  two  methods  described 
below  may  be  employed. 

1.  A  small  piece  (about  the  size  of  a  pea  or  beau  )  of  the 
tissue  may  be  inserted  under  the  skin  by  first  making  an 
incision  with  a  sharp  scalpel  through  the  .skin  and  superficial 
fascia,  and  then  with  a  pair  of  fine  forceps  insert  the  bit  of 
ti.ssue  well  under  the  skin  and  close  the  opening  with  one  or 
more  sutures. 

2.  The  tissue  may  be  crushed  in  a  mortar  and  thor- 
oughly mixed  with  a  few  cubic  centimeters  of  sterile  water  or 
bouillon  and  then  injected  with  a  hypodermic  syringe.  The 
needle  should  be  of  large  calibre.  If  it  is  suspected  milk,  it 
may  be  injected  into  the  abdominal  cavnty.  If  the  material  is 
tuberculous  and  contains  living  tubercle  bacteria,  the  death  of 
the  animal  follows  in  from  three  weeks  to  four  months. 
Usually  the  lymphatic  glands  in  the  groin  and  axilla  are  en- 
larged and  often  caseous.  If  a  guinea  pig  is  used,  the  liver, 
spleen,  lungs  and  kidneys  are  liable  to  be  affected,  in  the 
order  named  ;  if  a  rabbit,  the  lungs  are  often  the  first  of  the 
viscera  to  be  attacked. 

In  avian  tuberculosis  it  is  necessary  to  use  chickens 
instead  of  guinea  pigs.  They  may  be  inoculated  subcutane- 
ously  or  into  the  abdominal  cavity.  Several  weeks  may  be 
necessary  for  the  di.sease  to  develop  sufficiently  to  distingui.sh 


TUBERCULIN    TEST  215 

the    lesions    or    to    enable    one    to    find    the    bacteria    micro- 
scopically. 

§  155.  Tuberculin  test.  The  tuberculin  test  is  the 
best ''  and  in  a  large  majority  of  tuberculous  cases  among 
animals  and  in  man,  the  only  means  of  positively  detecting 
the  disease  in  the  living  individual. 

Tuberculin  Tuberculin  is  the  concentrated  liquid,  us- 
ually o-lvcerinated  bouillon,  on  which  tubercle  bacteria  have 
grown\;ntil  the  products  resulting  from  their  multiplication 
have  become  imparted  to  the  medium  in  sufficient  quantity  to 
inhibit  their  funher  development.  It  is  not  definitely  deter- 
mined just  what  these  products  are  or  just  how  they  are 
elaborated.  Briefly  stated,  the  preparation  of  tuberculin  con- 
sists in  the  following  procedure: 

I  The  preparation  of  the  culture  medium  i  glycerinated 
bouillon.,  distributing  it  m  suitable  flasks  and  inoculating  it 
with  the  growth  from  a  pure  culture  of  tubercle  bacteria. 

.  The  flasks  are  placed  in  an  incubator  at  a  temperature 
of  about  ^.7=  C.  where  they  remain  until  the  growth  ceases. 
The  lenc^ih  of  time  necessary  to  accomplish  this  depends  upon 
the  ac^e  and  condition  of  the  culture  from  which  the  inocula- 
tions were  made.       From   four  to   ten  weeks  are  usually   re- 

quired. 

^  \fter  the  maximum  growth  is  attained,  the  cultures 
are  sterilized  by  heat,  either  by  boiling  in  a  closed  water  bath 
or  heating  to  a  higher  temperature  in  an  autoclav. 

,  \fter  sterilization,  the  cultures  are  filtered  to  remove 
all  of  the  dead  bacteria,  and  then  the  filtrate  is  evaporated 
over  a  water  bath  to  the  desired  degree. 

,  The  concentrated  liquid  is  passed  through  a  Pasteur 
or  Berkefeld  filter,  standardized,  bottled  and  labeled  tor  dis- 
Uibution  It  should  be  perfectly  clear  although  its  color  may 
varv      If  it  is  cloudy  it  should  be  rejected. 

'  It  will  be  seen  from  the  method  of  preparation  that  tviber- 
culin  cannot  possibly   contain  living  tubercle  bacteria.     It  is 


2l6  TUBERCULOSIS 

heated  on  two  occasions  to  a  temperature  and  for  a  length  of 
time  far  in  excess  of  that  required  to  destroy  them,  besides  be- 
ing passed  through  a  filter  capable  of  removing  all  bacteria. 

The  original  tuberculin  or  lymph  of  Koch  was  concen- 
trated to  one-tenth  of  the  volume  of  the  saturated  culture. 
This  gave  a  thick,  syrupy  liquid  owing  to  the  presence  of  the 
glycerin.  The  diagnostic  dose  which  came  to  be  recom- 
mended for  cattle  of  medium  weight  was  0.25  c.c.  On  ac- 
count of  its  consistency  as  well  as  the  minuteness  of  the  dose, 
it  was  found  to  be  practicable  to  dilute  this  quantity  with 
seven  parts  of  a  diluent.  A  weak  solution  of  carbolic  acid 
was  ordinarily  used.  The  difficulties  and  the  danger  of  con- 
tamination involved  in  making  the  dilutions  in  the  field  led  to 
the  method  of  diluting  the  tuberculin  in  the  laboratory  before 
sending  it  out.  This  has  been  the  practice  of  the  Bureau  of 
Animal  Industry  for  a  number  of  years.  Equally  as  good  re- 
sults are  obtained  by  concentrating  the  saturated  culture  to 
the  point  where  2  c.  c.  contains  an  equivalent  of  the  0.25  c.  c. 
of  the  highly  concentrated  lymph.  This  process  avoids  the 
necessity  of  dilutions  and,  with  the  addition  of  a  few  drops  of 
carbolic  acid,  the  weaker  solution  keeps  perfectly. 

Tuberculin  in  the  dose  necessary  to  bring  out  its  diag- 
nostic effect  is  harmless  for  healthy  animals.  Thousands  of 
observations  that  have  been  reported  assure  us  of  this  fact. 
Tuberculin  is  in  daily  use  in  every  state  in  the  Union,  in 
Canada  and  in  every  country  of  Europe,  yet  so  far  as  can  be 
learned  not  a  single  case  of  injury  following  its  use  has  been 
reported.  In  the  tuberculous  animal  it  produces  a  rise  of  tem- 
perature which,  within  certain  limits,  follows  a  definite  course 
usually  terminating  in  from  18  to  24  hours  after  the  injection. 
Occasionally  the  temperature  remains  above  the  normal  for  a 
•longer  time.  The  temperature  usually  begins  to  rise  in  about 
eight  hours  giving  a  steady  but  quite  rapid  elevation  for  from 
I  to  3  hours,  a  continuous  high  elevation  for  from  2  to  4  hours, 
possibly  longer,  and  a  gradual  decline.  This  is  practically 
constant,  be  the  raise  moderate  or  extreme.  In  addition  to 
the  elevation  in   temperature   there   is   sometimes   a    marked 


TUBERCULIN    TEST  217 

nervous  chill.      Why  we  get  this  reaction-^-   is  not   positively 
determined. 

Applying  the  tuberculin  test.  In  brief,  the  method  for 
applying  the  tuberculin  test  in  cattle  is  as  follows  : 

1.  The  normal  temperature  of  the  animal  to  be  tested 
must  be  determined.  It  is  recommended  that  it  be  taken 
hourly  or  every  two  hours  for  the  day  preceding  the  test.  In 
practice  veterinarians  usually  take  the  temperature  but  once 
or  twice  before  injecting  the  tuberculin. 

2.  The  tuberculin  is  injected  subcutaneously  in  the  side 
of  the  neck.  Care  must  be  taken  that  the  syringe  is  sterile 
and  the  site  of  injection  should  be  disinfected.  The  size  of  the 
dose  depends  upon  the  preparation  of  tuberculin,  that  is,  the 
degree  of  concentration. 

*Trudeau  {Johns  Hof^khis  Hospital  BiiltetiH,  July ,  1S99)  gives  the 
following  summary  of  the  mechanism  of  the  tuberculin  reaction.  "The 
most  generally  accepted  theory  at  present  in  regard  to  it  is,  briefly,  the 
small  dose  of  tuberculin  injected  is  a  partly  speciiic  irritant  both  to 
tuberculous  foci  and  to  the  susceptible  organism  in  general.  It  pro- 
duces intense  hyperemia  of  all  tuberculous  tissue  in  the  body  (local 
reaction),  and  as  the  result  of  this  hyperemia  much  toxin  stored  up  in 
the  tubercles  themselves  is  thrown  into  the  general  circulation  and  pro- 
duces fever  and  characteristic  symptoms  which  go  to  make  up  what  is 
termed  'a  general  reaction.'  That  these  poisons  stirred  up  in  the  tuber- 
cles are  in  part  at  least  derived  from  the  dead  or  weakened  bacilli  has 
been  shown  by  the  experiments  of  Babes  and  Proca,  who  found  that  if 
two  sets  of  rabbits  be  injected  with  equal  quantities  of  living  and  dead 
bacilli,  the  latter  react  to  the  tuberculin  test  at  a  much  earlier  period 
than  those  inoculated  with  living  germs.  This  hypothesis  that  the  gen- 
eral reaction  is  brought  about  by  toxins  already  stored  up  in  the  tuber- 
culous lesions  and  exploded  as  it  were  by  the  hyperemia  produced 
about  these  lesions  as  the  result  of  the  test  of  injection  of  tuberculin,  is 
borne  out  by  the  fact  that  a  greater  amount  of  albumose  can  be  recov- 
ered from  the  evaporated  urine  collected  during  the  reaction  than  was 
contained  in  the  test  injection  also  by  clinical  observations  which  indi- 
cate that  patients  suffering  from  localized  surgical  tuberculous  processes 
of  limited  extent,  and  where  the  vascular  supply  to  the  part  is  limited, 
required  a  larger  test  injection  to  produce  the  reaction  than  those  who 
have  extensive  or  scattered  visceral  lesions  in  highly  vascular  organs 
like  the  lungs."  The  reader  is  referred  to  this  paper  for  a  careful  con- 
sideration of  the  vexed  questions  relating  to  tuberculin. 


2l8  TUBERCULOSIS 

3.  Beginning  6  or  S  hours  after  the  injection,  the  tem- 
perature should  be  taken  hourly,  or  at  least  every  two  hours, 
for  fully  three-fourths  of  a  day. 

4.  During  the  time  of  testing,  the  cattle  should  be  kept 
quiet  and  free  from  all  exposure,  and  fed  normally. 

5.  In  case  of  reaction,  there  should  be  a  rise  of  at  least 
1.5°  F.  above  the  maximum  individual  normal  temperature  as 
determined  on  the  preceding  day.  The  elevation  should  come 
on  gradually,  remaining  practically  at  its  fastigium  for  a  few- 
hours  and  gradually  subside.  Erratic  elevations  of  short  dura- 
tion are  to  be  excluded.  In  cases  of  doubt  the  animals  should 
be  retested. 

6.  Animals  advanced  in  pregnancy  and  those  known  to 
be  suffering  from  any  other  disease  or  in  oestrum  should  not  be 
tested.  All  methods  of  treatment,  including  exposure  to  cold, 
or  kind  of  food  and  drink  which  would  tend  to  modify  the 
temperature,  should  be  avoided.  Animals  in  which  the  disease 
is  far  advanced  sometimes  fail  to  react. 

7.  The  dose  should  vary  to  correspond  with  the  weight 
of  the  animal.  The  dose  for  an  adult  cow  of  average  weight  is 
0.25  c.c.  of  the  concentrated  Koch  tuberculin.  In  cases  of  a 
second  test  within  a  few  days,  the  quantity  of  tuberculin 
injected  should  be  larger  than  for  the  first  test. 

Ward  has  pointed  out  the  fact  that  fowls  do  not  give  a 
diagnostic  reaction  to  tuberculin  made  from  either  the  avian  or 
mammalian  varieties  of  the  tubercle  bacteria. 

In  cattle  there  is  a  marked  variation  in  the  normal  daily 
temperature.  A  fluctuation  of  two  or  even  three  degrees 
within  24  hours  is  frequently  found.  Cold  water  when  drunk 
in  considerable  quantities  lowers  the  temperature  from  two  to 
four  degrees.  A  temporary  excitement  usually  causes  an  eleva- 
tion of  from  I  to  1.5°  F.  There  are  also  marked  variations  in 
the  temperature  of  the  same  animal  on  consecutive  days.  The 
temperature  at  12  noon  and  12  midnight  are  often  the  same. 
In  some  cases  the  maximum  elevation  for  the  day  occurs  near 
midnight  and  on  the  following  day  the  minimum  temperature 
appears  at  that  time.     It  is  not  uncommon  for  the  maximum 


TrHP:RCULIN    TEST  219 

temperature  to  occur  twice  in  the  same  daj-  and  occasionally 
several  times  within  the  twenty-four  hours.  There  are  marked 
individual  variations  in  the  effect  of  ordinary  conditions  upon 
the  temperature,  such  as  food,  excitement  or  temperature  of 
the  air.  A  hot  spell  causes  a  rise  of  two  and  in  some  cases 
four  degrees.  The  average  temperature  of  the  animals  in 
three  herds  tested  by  Howe  and  Ryder  were  102.5°,  102.6°, 
and  101°  F.  respectively. 

In  a  well  kept  Government  herd  that  was  tested  with 
tuberculin,  the  temperature  of  part  of  the  animals  was  taken 
hourly  for  24  and  part  of  them  for  16  hours  preceding  the 
Injection.  An  examination  of  the  records-i^  shows  the  average 
daily  variation  of  20  animals  in  which  the  temperature  was 
taken  for  24  hours  to  be  2.31°  F.  The  maximum  individual 
variation  in  a  single  day  was  4.3°  F". ,  the  minimum  0.5°  F. 
In  25  other  animals  where  the  temperature  was  taken  for  16 
hours,  the  average  variation  was  1.79°  F.  In  these  the  maxi- 
mum variation  was  3.2°  F.,  the  minimum  0.6°  F.  Ten 
healthy  animals  (did  not  react  to  tuberculin)  in  the  same  herd 
gave  an  average  variation  of  2.08°  F.  In  these  the  maximum 
daily  variation  was  4.1°  F.,  the  minimum  1°  F.  The  lowest 
temperature  was  usually,  but  not  invariably,  in  the  morning 
and  the  highest  in  the  afternoon  or  evening.  I  have  appended 
the  records  of  the  temperature  of  two  of  these  animals. 


^Bulletin  No.  7,  Bureau  of  Animal  Industry,  U.  S.  Department  of 
Agriculture,  Washington,  D.  C.  The  tests  were  made  by  Drs.  F.  L. 
Kilborne  and  E.  C.  Schroeder,  under  the  direction  of  Dr.  Theobald 
Smith. 


TUBERCULOSIS 


THE  INITIAI,  TEMPERATURE  OF    TWO    COWS,   WITH    RATE    OF     PUI.SE 
AND  NUMBER  OF  RESPIRATIONS  PER  MINUTE. 


Cow    No.  I 


Cow    No.  2 


Tempera- 
ture 


Pulse      Resp. 

I 


Tempera- 
ture 


Pulse      Resp. 


9  A.  M. 

99.8 

48 

18 

98.6 

48 

15 

!0   " 

99-5 

66 

18   1 

98.6 

66 

15 

II   " 

99.0 

60 

^5 

99.0 

60 

15 

12   " 

100.8 

54 

15   1 

99-4 

54 

15 

I  P.  M. 

101.4 

54 

15 

lOO.O 

54 

18 

2   " 

101.6 

48 

15 

100.2 

54 

18 

3  " 

102.0 

60 

24 

100.4 

72 

24 

4  " 

103.0 

66 

24 

102.7 

72 

24 

5  " 

103-3 

66 

24 

102.8 

72 

27 

6  " 

103.1 

57 

18 

103.0 

60 

27 

7  " 

102.2 

60 

20 

102.4 

60 

24 

8  " 

103.0 

56 

16 

102.0 

60 

24 

9  " 

103. 1 

52 

24 

102.2 

50 

24 

lO   " 

102.5 

60 

20 

102.0 

50 

IS 

II  " 

102.5 

60 

20   1 

102.0 

60 

20 

12  midnight 

102.4 

56 

16 

IOI.6 

54 

20 

I  A.  M. 

101.8 

60 

20   1 

101.4 

^8 

24 

2   " 

102.0 

64 

18 

102.2 

58 

18 

3  " 

102.0 

60 

18 

101.6 

38 

18 

4  " 

102.2 

54 

24 

101.5 

60 

24 

5  " 

101.6 

56 

24 

102.0 

60 

18 

6  " 

101.8 

60 

18 

102.2 

60 

20 

8  " 

102.5 

56 

16   1 

103.2 

60 

18 

In  view  of  these  normal  temperature  variations,  which 
often  exceed  the  tuberculin  reaction,  it  is  obvious  that  before 
applying  the  test  the  normal  temperature  of  the  animals  should 
be  approximate!}^  determined  and  that  when  thej-  are  being 
subjected  to  the  test  they  should  be  cautiously  protected, 
otherwise  the  comparativeh'  slight  elevation  necessary  to  detect 
the  disease  may  be  disguised. 

As  the  reaction  seems  to  be  the  result  of  an  affinity  exist- 
ing between  the  tuberculin  and  the  living  tuberculous  lesion, 
it  is  natural  to  suppose  that  when  the  two  are  brought  together 
in  the  same  animal  it  would  invariably  take  place.  Experience 
has  shown  that  it    almost    always    does.      It    is    important    to 


TUBERCULIN    TEST  221 

understand,  as  far  as  possible,  the  reason  for  the  exceptions 
and  the  extent  to  which  they  occur.  The  reported  failures  of 
the  tuberculin  tests  fall  into  two  distinct  classes. 


7/m/rs      Aft 

r.r     1  yi 

' e.rfn  c 

{ 

r 

? 

/C 

/^ 

/6' 

/r 

^r? 

/07" 

^^■^ 

"-^ 

i5 

} 

-^ 

^^^ 

^ 

,  00' 

—7h 

^ 

"^ 

■^^^ 

/  o-^' 

3/y 

"■" 

/y 

.    03' 

^ 

C^" 

^ 

1 

.'O/^ 

^ 

.-^  teuipenxtuie  curve  of  three  cows  after  injecting  tuberculin. 
I  a  healthy  cozu,  2  and  j  tuberculous  ones. 


■^.00 

s:io 

XSO 

.5:  JO 

.S'.f-O 

s.so 

a./o 

■7.00 

S.Oo 

r 

/03 

lOZ 

.^^ 

i^^AN 

H  rRi 

'ELY 

or  //a 

TCR     4 

T  39' F 

100 

\ 

^ 

— 

99 

^\ 

_^ 

,^^ 

Fig.  52.     Chart  shoiviug  the  effect  of  drinking  cold  water  upon  the 
tetnperature  of  a  coiv. 

I.  There  is  a  reaction  and  no  disease  is  found.  In 
explaining  this  alleged  error,  the  records  of  the  cases  which 
have  come  to  my  attention  have  been  so  deficient  in  data  con- 
cerning the  normal  temperature  variation  of  the  animals,   and 


TUBERCULOSIS 


the  incompleteness  of  the  post-mortem  examinations,  that  it 
seems  possible  for  the  error  to  rest  with  the  observer  quite  as 
much  as  with  the  tuberculin.  Unfortunatel}-  we  are  as  yet 
unable  to  determine  by  the  reaction  the  extent  of  the  disease, 
so  that  a  beg^inning  lesion  no  larger  than  a  walnut  may  cause 
a  pronounced  rise  of  temperature  and  such  a   tubercle  may   be 


/ 

^ 

A.M. 

.3    4 

S 

^ 

/^ 

F 

A.M 
9  /r 

// 

/a" 

7 

^ 

3    V 

s 

f 

^ 

. 

/'M 
9  /< 

//  //- 

/06./i 

\ 

/Ot. 

-— - 

\ 

\ 

/OS.  P 

\ 

\ 

/OJ^ 

/Cd^ 

. 

f; 

1 

/ 

\ 

/c.:j. 

1 

/  \l 

/(■/./ 

1 

/ 

^ 

/c-/.e 

1 

/ 

A  v./ 

1 

/C-^.K 

1 

/r4 

1^ 

/cm 

/ 

/03.^ 

/ 

/^^/ 

r^ 

^ 

/C^.6 

^ 

y 

■v. 

-— 

/0^.4 

M/\ 

'^Ch 

\ 

/0<f.<^ 

■— 

-, 

/ 

\ 

, 

c' 

/r^. 

/ 

^ 

-'' 

/C/.  P 

y' 

/f/.  (: 

AM 

K'H 

^O 

/C/4 

\ 

,/\ 

/ 

/Cf-  s 

/c/. 

1       ^ 

/ 

Fig.  53.      Temperature  curve  of  a  hog.     Dotted  litie  A    represents   temper- 
ature of  a  hog  for  24  hours  before  the  injection  of  tuberculin.       The 
full  line  B  represents  the  temperature  of  t/ie  hog  for  .?/ 
hours  after  the  injection  of  tuberculin  {Schroeder). 

difficult  to  find,  especially  if  located    in   the    marrow    of  some 
bone  or  in  the  nervous  system. 

2.  There  is  no  reaction  and  the  disease  exists.  It  is 
generally  admitted  that  advanced  cases  often  fail  to  react,  but 
here  the  test  itself  is  of  little  importance,  as  the  disease  can 
be  detected  by  the  clinician  on  physical  examination.  When, 
however,  tuberculin  is  carefully  prepared  and  scientifically 
administered,  these  exceptions  are  exceedingly  rare.  It  seems 
to  act  always  in  active  tuberculosis. 


TUHERCULIN    TEST 


223 


Tuberculin  does  not  give  a  reaction  during  the  period  of 
incubation.  It  does  not  cause  a  reaction  in  many,  if  not  all, 
cases  of  temporary  arrest  or  healing  of  the  lesions.  This  ren- 
ders it  difficult  to  interpret  the  negative  results  especially  in 
herds  where  there  are  many  positive  reactions.  In  such  cases 
there  should  be  subsequent  tests  later.  For  this  reason  cattle 
bought  on  the  tuberculin  test  can  not  be  considered  uninfected 


tiouRs  ArrER  Injection 


'Fig.  54.     Irregular  temperatures  follozving  tuberculin  that  arc  >iot  caused 
by  tuberculosis  [Curtice). 

as  the  result  of  the  first  test  if  they  came  from  herds  contain- 
ing reacting  animals. 

The  practical  value  of  tuberculin  lies  in  its  efficiency  in 
the  arts  of  comparative  and  sanitary  medicine.  It  is  in  the 
practical  application  that  difficulties  are  encountered.  The 
many  details  and  precautions  enumerated  as  absolutely  essen- 
tial to  the  best  results  are  often  considered  too  tedious  and 
time  consuming,  and  consequently  the  practice  has  come  too 
generally  into  vogue  of  neglecting  or  ignoring  many  of  the 
precautions.  In  order  that  the  test  may  be  practicable,  some 
practitioners  resort  to  a  shorter  method  of  procedure  even  at 
the  risk  of  an  occasional  error. 

§  156.  Prevention.  Tuberculosis,  like  other  infectious 
diseases,  can  be  very  largely   prevented.     To  accomplish  this 


224 


TUBERCULOSIS 


it  is  necessary  to  keep  tuberculous  animals  from  entering  the 
healthy  herds.  If  they  are  admitted  and  later  the  fact  is  dis- 
covered, it  is  necessary  to  remove  them  and  to  thoroughly  dis- 
infect the  stable.  In  eliminating  the  disease  from  a  herd  by 
means  of  the  tuberculin  test,  it  is  necessary  to  retest  the  non- 
reacting  animals  after   six  months  or  a  year  have  passed  in 


A.M. 

9  00 

P.M. 
1  oo 

^oo 

A.M. 

^oc^ 

I0  6 

/ 

^^^^ 

y' 

\ 

/ 

\ 

5 
/04- 

/ 

\6- 

/ 

\ 

I03 

/ 

\ 

k^ 

/ 

V 

\^ 

/OX 

V 

/  \ 

\ 

MAf^CH 

/6 

// 

-- — . 

^ 

s 

\ 

/ 

'A 

""--- 

— 4_ 

.--^ 

\fr 

/ 

y 

s 

\ 

r 

A 

/ 

s 

-4,„ 

<    /S 

' ; 

m 

Fig.  55.  Temperature  curve  of  a  tuberculous  cow  for  48  hours.  The  line 
A.  A.  s/iozas  temperature  for  24  hours  preceding-  the  injection  of  tuberculin, 
which  ivas  injected  at  g.  A.  M.,  March  16  ;  b,  b,  b,  shorvs  the  temperature 
for  the  24  hours  after  the  tuberculin  injection. 

order  to  find  any  case  that  might  have  been  infected,  but  in 
which  the  disease  had  not  begun  to  develop,  or  cases  that  were 
temporarily  healed  at  the  time  of  the  first  test. 

§  157.  The  control  of  tuberculosis  in  cattle.  Several 
methods  have  been  proposed  to  eliminate  tuberculosis  from 
cattle.  The  preventing  of  the  spread  of  the  virus  from  the 
diseased  to  the  healthy  animals  is  the  most  important  precau- 
tions. The  system  introduced  by  Prof  Bang  of  Copenhagen, 
Denmark,  and    generally    known    as   the    Bang    method,    has 


REFERKNCES  225 


proven  to  be  most  successful.  It  consists  in  the  slaughter  of 
the  advanced  cases  and  the  isolation  of  the  reacting  animals, 
which  are  kept  for  breeding  purposes.  The  calves  are  .sepa- 
rated from  their  dams  immediately  after  birth  and  fed  upon 
the  milk  of  healthy  cows  or  the  sterilized  milk  of  the  reacting 
ones.  This  method  has  enabled  many  owners  of  infected 
animals  to  replenish  their  herds  in  from  four  to  six  years.  In 
countries  where  it  has  been  generally  applied  the  percentage 
of  tuberculous  cattle  has  been  wonderfully  reduced. 

The  vaccination  of  cattle  against  tuberculosis  has  been 
proposed  as  a  prophylactic  measure.  The  method  has  been 
extensively  tried  by  Pearson  in  x\merica  and  von  Behring  in 
Germany.  Its  effectiveness  can  not  be  predicted  at  this  time. 
The  results  of  von  Behring's  experiments  are  promising  but 
as  yet  the  vaccinated  animals  (calves)  have  not  attained  to  old 
age  so  that  the  length  of  the  resistance  that  seems  to  be 
established  by  the  vaccination  is  not  determined.  Several 
reports  on  the  result  of  natural  exposure  to  tuberculous  cows, 
after  a  period  of  two  years,  show  the  vaccinated  animals  to 
be  nearly  as  badly  infected  as  the  checks.  The  resul  ts  reported 
by  Pearson  indicate  that  the  attainment  of  a  bacterial  immunity 
against  tuberculosis  in  cattle  is  not  likely  to  be  an  easy  task. 
The  experiments  in  this  direction  are  most  interesting  and 
many  investigators  are  hopeful  for  good  results.  At  present 
it  is  in  the  experimental  stage. 


REFERENCES. 


1  \DAMi  On  the  significance  of  bovine  tuberculosis  and  its 
eradication  and  prevention  in  Canada.  Ca>iadia>,  Jour,  of  Medicine 
and  Surgery,  Dec.  1899. 

2  Curtice.  The  detection  of  tuberculosis  in  cattle.  Annual 
Report,  Bureau  of  Animal  Industry,  U.  S.  Dept.  Agric.,  1895-96- 

3.  Dorset.  Experiments  concerning  tuberculosis.  Bulletin  5.'. 
Bureau  of  Animal  Industry,  1904. 

4  Eber  Suggestions  for  a  uniform  system  of  interpreting  the 
tuberculin  reaction  in  cattle.  The  Jour.  ComPr.  Path,  and  Ihcra., 
Vol.  XVIII  (1905),  P-  224. 


226  TUBERCULOSIS 

5.  Koch.  The  etiology  of  tuberculosis.  Mitt,  aus  dem.  Kaiserl. 
GesiindhcUsamte,  Vol.  II  ( 1884).  Translated  in  Vol.  CXV,  New  Syden- 
ham Society. 

6.  Koch.  The  combating  of  tuberculosis  in  the  light  of  the  exper- 
ience that  has  been  gained  in  the  successful  combating  of  other  infec- 
tious diseases.     Amer.  Vet.  Rev.,  Vol.  XXV  (1901),  p.  44i- 

7.  MoHLER.  Infectiveness  of  milk  of  cows  which  have  reacted  to 
the  tuberculin  test.     Bulletin  44.     Bureau  of  Animal  hidiistry,    1903. 

8.  MOHLER  AND  Washburn.  A  comparative  study  of  tubercle 
bacilli  from  varied  sources.  Bulletin  96.  Bureau  of  Animal  Indus- 
try, 1907. 

9.  MOHLER.  Tuberculosis  in  hogs,  with  special  reference  to  its 
suppression.     Amer.  Vet.  Rev.,  Vol.  XXXII  (1907),  P-  176. 

ID.  Moore  and  Dawson.  Tuberculosis  in  swine,  the  nature  of  the 
disease  with  a  report  of  three  cases.  Annual  Report,  Bureau  of  Ani- 
mal Industry,  U.  S.  Dept.  Agric,  1895-96. 

1 1.  Moore.  The  preparation  of  tuberculin,  its  value  as  a  diagnostic 
agent,  and  remarks  on  the  human  and  bovine  tubercle  bacilli.  Trans, 
of  the  Med.  Society  of  the  State  ofN.  Y.,  1900. 

12.  Moore,  a  report  on  bovine  tuberculosis.  Nezc  York  State 
Dept.  of  Agric.,  1903. 

13.  NOCARD.     The  animal  tuberculosis.     New  York. 

14.  Pearson.  The  Pennsylvania  plan  for  controlling  tuberculosis 
of  cattle.     Proc.  Amer.  Vet.  Med.  Assn.,  1899. 

15.  Pearson.  Tuberculosis  in  cattle  and  the  Penn.  plan  of  its 
repression.     Bulletin  75.     Pemi.  Dept.  of  Agric,  1901. 

16.  Pearson.  The  repression  of  tuberculosis  in  cattle  by  sanita- 
tion.    Bulletin  J4.     Penn.  Dept.  of  Agric,  190 1. 

17.  Pearson.  The  artificial  immunization  of  cattle  against  tuber- 
culosis.    Amer.  Vet.  Rev.,  Vol.  XXIX  (1905),  p.  543- 

18.  Ravenei,.  The  dissemination  of  tubercle  bacilli  by  cows  in 
coughing  a  possible  source  of  contagion.  Univ.  of  Penn.  Med.  Maga- 
zine, Nov.   1900. 

19.  Ravenel.  The  comparative  virulence  of  the  tubercle  bacillus 
from  human  and  bovine  sources.  Univ.  of  Penn.  Med.  Bulletin 
Sept.,  1901. 

20.  Ravenel.  The  intercommunicability  of  human  and  bovine 
tuberculosis.     The  Univ.  of  Penn.  Med.  Bulletin  May,  1902. 

21.  Repp.  Transmission  of  tuberculosis  through  meat  and  milk. 
American  Medicine,  Oct.  6,  Nov.  2,  1901. 

22.  Salmon.     Legislation  with  reference  to  bovine  tuberculosis. 


REFERENCES  227 

Bulletin  2S.     Bureau  of  Animal  Industry,  U.  S.  Dcpl.  of  Agric,  1901. 

23.  vSalmon.  The  tuberculin  test  of  imported  cattle.  Bulletin  ?.'. 
Bureau  of  Animal  Industry,  U.  S.  Dept.  of  .I'^ric,  1901. 

24.  Salmon.  Bovine  and  human  tuberculosis.  Procecdiiii^s 
.Inter.  Vet.  Med.  .Isso.,  1903,  p.  436- 

25.  Salmon.  Tuberculosis  of  the  food-producing  animals. 
Bulletin  jS.     Bureau  of  Animal  Industry,  1906. 

26.  SCHROEDER  AND  CoTTON.  The  relation  of  tuberculous  le- 
sions to  the  mode  of  infection.  Bulletin  gj.  Bureau  of  Animal  Indus- 
try, 1906. 

27.  SCHROEDER  AND  CoTTON.  Experiments  with  milk  artificially 
infected  with  tubercle  bacilli.  Bulletin  S6.  Bureau  of  Animal  Indus- 
try, 1906. 

28.  SCHROEDER  AND  MOHLER.  The  tuberculin  test  of  hogs. 
Bulletin  8S.     Bureau  of  Animal  Industry,  1906. 

29.  vSmiTh.  Investigations  concerning  bovine  tuberculosis  with 
special  reference  to  diagnosis  and  prevention.  (Pathological  part). 
Bulletin  No.  7,  Bureau  of  Animal  Industry,   U.    S.    Dept.    of  Agric, 

1894. 

30.  Smith.  A  comparative  study  of  bovine  tubercle  bacilli  and  of 
human  bacilli  from  sputum.     The  four,  of  Ex  per.  Med.,  Vol.  Ill  (J898). 

31.  vSmiTh.  The  thermal  death  point  of  tubercle  bacilli  in  milk 
and  some  other  fluids.  The  four,  of  Exper.  Med.,  Vol.  IV  (1899), 
p.  217. 

32.  Smith.  The  channels  of  infection  in  tuberculosis,  together 
with  some  remarks  on  the  outlook  concerning  a  specific  therapy. 
Trans.  Mass.  Med.  Soe..  1907. 

REFERENCES   TO   AVIAN   TIHERCULOSIS 

33.  Burnett.  Tuberculosis  in  chickens  positively  identified  in 
New  York.     Am.  Vet.  Revieiv,  XXX  (1907),  P-  1312. 

34.  Brav.  Tuberculosis  in  chickens,  four.  Compar.  Med.  and 
Vet.  Archives,  XVII  (1896),  p.  461. 

35.  CadioT.  Bur  la  tuberculose  du  cygne.  Bui.  de  la  Soe.  Cen.  et 
Med.  Vet.,  Vol.  XLIX  (1895),  P-  57°. 

36.  CadioT,  Gilbert  and  Roger.  Inoculation  of  the  tubercu- 
losis of  gallinaceous  to  mammalia.     Amer.  Vet.  Bevierc,  XX    (1896-7), 

p.  225. 

37  CADIOT  Gilbert  et  Roger.  Note  sur  la  tuberculose  des 
volailles.     I^eeeuil  de  Med.  Vet.  Serie  VII,  Vol.  VIII  (1891),  p.  22. 

38.     CadioT,  Gilbert  and  Roger.     A  contribution  to  the  study  of 


228  TUBERCULOSIS 

avian  tuberculosis.     vStudies  in  clinical  veterinary  medicine  and  surgery. 
(1900).     (Translated  by  Dollar.) 

39.  EbkrlEin.  Die  Tuberculose  der  Papageien.  Monatshefte  fi'ir 
Praktische  Thierheilktmde,  Bd.  V  (1894),  S.  248. 

40.  Froehner.  Zur  Statistik  der  Verbreitung  der  Tuberculose 
unter  den  kleinen  Hausthieren.  Monatshefte  fur  Praktische  Tierheil- 
kunde,  1893,  p.  51. 

41.  LuCET.  Sur  un  symptome  de  la  tuberculose  chez  la  poule. 
Rccueilde  Med.  Vet.,  Serie,  VI f,  Vol.  VIII  (1891),  p.  172. 

42.  Maffucci.  Die  Huhnertuberculose.  Zeitschr.fiir  Hygiene, 
Bd.  XI  (1892),  p.  445- 

43.  Moore  and  Warp.  Avian  tuberculosis.  Proc.  Auier.  Vet. 
Med.  Asso.,  1903,  p.  169. 

44.  Moore.  The  morbid  anatomy  and  etiology  of  avian  tuber- 
culosis.   Jour,  of  Med.  Research,  Vol.  XI  (1904),  p.  5' 2  (Bibliography.) 

45.  Nocard.  Sur  une  tuberculose  zoogleique  des  oiseaux  de 
bassecour.  But.  et  Memoires  de  la  Sac.  Centrale  ct  Med.  Vet.,  1885, 
p.  207. 

46.  Nocard.  Transmission  de  la  tuberculose  des  poules  et 
I'homme.      Veterinaire,  Vol.  Ill  (1886),  p.  658. 

47.  PernoT.  Investigatiousof  diseases  of  poultry.  Bulletin  No.  64. 
Oregon  Agric.  Expt.  Sta.,  1900. 

48.  SiBivEY.  Tuberculosis  in  birds.  Jour,  of  Coinpar.  Med.  and 
Vet.  Arch.,  Vol.  XI  (1890),  p.  317- 

49.  Straus  et  Gamaleia.  La  tuberculose  humaine,  sa  distinc- 
tion de  la  tuberculose  des  oiseaux.     Archiv.  de  Med.    Exper.,   Bd.    Ill 

(1891),  p.  457. 

50.  Straus  et  WurTz.  Sur  la  resistance  des  poules  a  la  tubercu- 
lose par  ingestion.     Congress  pour  V  etude  de  la  tuberculose,  1888,  p.  28. 

51.  Ward.  Tuberculosis  in  Fowls.  Bulletin  No.  161  California 
Agr.  Exper.  Station,  1904. 

52.  Weber.  Review  of  the  avian  tuberculosis.  Jour,  of  Compar. 
Med.  and  Vet.  Arch.,\o\.  XIII  (1892),  p.  429. 

THE    FOLLOWING    BULLETINS    ON    TUBERCULOSIS     HAVE     BEEN 

ISSUED    FROM    THE    VARIOUS   STATE    AGRICULTURAL 

EXPERIMENT    STATIONS. 

Bang.  The  application  of  tuberculin  in  the  suppression  of  bovine 
tiiberculosis.     Bulletin  41.     Massachusetts.     1896.     (A  translation). 

Beach.  The  history  of  a  tuberculous  herd  of  cows.  Bulletin  24. 
Storrs,  Conn.  1902. 


BULI.KTINS  229 

Bitting.     Bovine  tuberculosis  in   Indiana.   Bulletin  63.     Ind.    1S96. 

Brewer.     Tuberculosis.     Bulletin  41.     Utah.     1895. 

Carv.     Bovine  tuberculosis.     Bulletin  67.     Alabama.     1S95. 

CONX.  The  relation  of  bovine  tuberculosis  to  that  of  man  and  its 
significance  in  the  dairy  herd.     Bulletin  25.     Storrs,  Conn.     1902. 

DiNWiDDiE.  The  relation  of  virulence  for  the  domestic  animals  of 
human  and  bovine  tuberculosis.     Bulletin  57.     Kansas.     1S99. 

DixwiDDiE.  The  relative  susceptibility  of  the  domestic  animals 
to  the  contagia  of  human  and  bovine  tuberculosis.  Bulletin  63. 
Kansas.     1900. 

Fischer.     Bovine  tuberculosis.     Bulletin     69.     Kansas.     1898. 

Glover.  Relation  of  bovine  to  human  tuberculosis.  Bulletin 
66.     Colorado.     1901. 

Grange.     Tuberculosis.     Bulletin  133.     Michigan.     1896. 

Harding,  Smith  and  Moore.  The  Bang  method  etc.  Bulletin 
277.     Geneva,  N.  Y.      1906. 

Hill  and  Rich.   Bovine  tuberculosis.   Bulletin  42.   Vermont.     1894. 

Law.  Tuberculosis  in  relation  to  animal  industry  and  public 
health.     Bulletin  65.      (Cornell) ,  New  York.     1894. 

Law.  Experiments  with  tuberculin  on  non-tuberculous  cows. 
Bulletin  81.      (Cornell),  New  York.      1894. 

Law.  Tuberculosis  in  cattle  and  its  control.  Bulletin  150. 
(Cornell],  New  York.     1898. 

iVL\RSHALL.  A  study  of  normal  temperatures  and  the  tuberculin 
test.     Bulletin  159.     Michigan.     1898. 

M.\rshall.  Killing  the  tubercle  bacilli  in  milk.  Bulletin 
173.     Michigan.     1899. 

Mayo.  Some  diseases  of  cattle,  Texas  itch,  blackleg,  tuberculosis. 
Texas  fever.     Bulletin  69.     Kansas.  1897. 

Moore.     Bovine  tuberculosis.  Bulletin  225.    (Cornell),  N.  Y.     1905. 

Nelson.  On  the  use  of  Koch's  lymph  in  the  diagnosis  of  tubercu- 
losis.    Report  of  the  biologist.     New  Jersey.     1893. 

Nelson.  Experimental  studies  of  the  Koch  test  for  tuberculosis. 
New  Jersey.     1895. 

Nelson.  The  suppression  and  prevention  of  tuberculosis  of  cattle 
and  its  relation  to  human  consumption.  Bulletin  118.  New  Jersey.   1896. 

Nf^om.     Tuberculosis  of  cattle.     Bulletin  50.     S.  C.     1900. 
Paige.     History  of  tuberculosis  in  a  college  herd.     Use  of  tubercu- 
lin in  diagnosis.     Bulletin  26.     Massachusetts.     1S94. 


230  JOHNE  S    DISEASE 

Pearson.     Tuberculosis  of  cattle.     Bulletin  29.     Penn.     1S94. 

REVNOtDS.  Bovine  tuberculosis.  Bulletin  51.  Univ.  of  Minn. 
Agric.  Exp.  Station.     1896. 

RisSELL.  Tuberculosis  and  the  tuberculin  test.  Bulletin  40. 
Wisconsin.     1S94. 

Russell.  The  history  of  a  tuberculous  herd  of  cows.  Bulletin 
78.     Wisconsin.     1899. 

Russell.  a  lesson  in  bovine  tuberculosis.  Bulletin  114.  Wis- 
consin.     J  904. 

Russell.  Two  ways  of  treating  tuberculosis  in  herds.  Bulletin 
136.     Wisconsin.     1905. 

Russell  and  Hastings.  Bovine  tuberculosis  in  Wisconsin. 
Bulletin  84.     Wisconsin.     1901. 

Stalker  and  NilES.  Investigation  of  bovine  tuberculosis  with 
special  reference  to  its  existence  in  Iowa.     Bulletin  108.     Iowa.     1S95. 

Thorne.     Bovine  tuberculosis.     Bulletin   108.     Ohio.      1899. 

Van  Es.  Bovine  tuberculosis.  Bulletin  77.  North  Dakota  Agri- 
cultural Experiment  Station.     1907. 

Williamson  and  Emery.  Tuberculosis  and  its  prevention. 
Bulletin  117.     N.  C.      1895. 


johne's  disease 

Synonyms.  Pseudo-tuberculosis  ;  chronic  bovine  pseudo- 
tuberculous enteritis  ;  La  diarrhee  chronique  du  boeiif. 

§  158.  Characterization.  Johne's  disease  is  an  intes- 
tinal disorder  supposed  to  be  due  to  acid-fast  bacteria.  It  is 
characterized  b}'  a  diarrhea,  gradual  emaciation  and  the  pres- 
ence of  large  numbers  of  acid-fast  bacteria  on  the  surface  of 
and  in  the  mucous'membrane  of  the  affected  portions  of  the 
intestine.  The  distal  part  of  the  ileum  is  usually  the  most 
involved. 

§  159.  History.  Johne  and  Frothingham  described  a 
disease  in  1895  in  which  the  intestinal  mucosa  contained  large 
numbers  of  acid-fast  bacteria.  They  thought  it  was  a  case  of 
tuberculosis  in  a  cow  due  to  the  avian  tubercle  bacterium.  In 
1903  Markus  called  attention  to  its  frequent  occurrence  in 
Holland.     Since  that  time  it  has  been  recognized  in  Belgium, 


MORUID    ANATOISIY 


231 


Switzerland,  Denmark  and  England.  A  few  cases  have  been 
observed  in  this  country.  Sir  John  M'Fadyean  has  proposed 
the  name  Johne's  disease  for  this  affection. 

j^  160.  Etiology.  The  cause  of  this  disease  is  suppo.sed 
to  be  an  acid-fast  bacterium  which  is  found  in  large  numbers 
in  the  affected  mucosa,  and  also  in  the  mesenteric  and  colic 
lymphatic  glands.  Morphologically  this  organism  closely  re- 
sembles the  tubercle  bacterium.  It  varies  in  size  from  i  to  2/.< 
in  length  and  a  few  are  said  to  attain  to  4//.  It  stains  uni- 
formly but  occasionally  the  longer  forms  show  alternating 
stained  and  unstained  segments.      It  is  remarkably  acid-fast. 

According  to  M'Fadyean  this  organism  is  not  inoculable 
to  either  guinea  pig  or  rabbits.  It  has  as  yet  not  been  culti- 
vated on  artificial  media. 

This  bacterium  apparently  does  not  form  a  strong  cell 
poison  and  hence  the  absence  of  necrosis.  On  the  other  hand 
the  tissues  appear  to  be  almost  powerless  to  restrain  its  multi- 
plication and  invasion. 

The  period  of  i7icubatioti  is  not  known. 

§  161.  Symptoms.  The  first  symptom  to  be  observed 
is  a  loss  of  flesh,  although  the  appetite  remains  normal.  The 
hair  becomes  roughened  and  the  animal  presents  an  unthrifty 
appearance.  Diarrhea  soon  sets  in.  As  a  rule,  the  diarrhea 
is  profuse  and  persistent  from  the  time  it  begins,  although  it 
may  sometimes  be  checked  temporarily  by  giving  dry  food 
and  by  the  administration  of  astringents. 

S  162.  Morbid  anatomy.  The  lesions  are  primarily  in 
the  small  intestines,  but,  as  a  rule,  involving  the  large  intes- 
tines, before  death  takes  place.  The  distal  part  of  the  small 
intestines  is  most  involved.  The  lesion  is  in  the  mucous 
membrane  and  even  in  seriously  ill  animals  it  is  the  only 
lesion  that  has  been  found.  In  some  cases  the  acid  fast  bac- 
teria invade  the  submucosa  in  which  ca.se  the  wall  of  the  in- 
testine becomes  thickened.  In  proportion  to  this  thickening 
the  mucosa  shows  more  or  less  coarse  wrinkling.  I'lceratiou 
is  not  ob-served,  and  there  is  very  little  congestion. 


232  JOHNE  S    DISEASE 

The  mesenteric  lymphatic  glands  ma}-  be  slightly  en- 
larged. When  cut  an  appreciable  amount  of  water-like  liquid 
exudes  from  the  surface.  The  absence  of  congestion  has  been 
noted. 

The  most  striking  feature  of  the  disease  is  the  slight 
tissue  changes  even  when  the  bacteria  are  exceedingly  num- 
erous. In  sections  made  at  right  angles  to  the  mucous  sur- 
face of  the  intestine  an  irregularity  in  the  size  and  outline  of 
the  villi  can  be  observed.  Some  of  the  villi  may  be  partially 
denuded  of  epithelium.  In  the  glandular  layer  the  inter- 
stitial tissue  between  the  tubular  glands  may  be  increased  in 
amount  and  the  glands  may  show  evidence  of  atrophy.  In 
sections  stained  by  the  Ziehl-Neelsen  method,  with  Pappen- 
heim's  stain  for  contrast,  M'Fadyean  states  that  those  parts 
in  which  the  bacilli  are  numerous  have  an  appearance  verj' 
similar  to  that  of  a  genuine  tuberculous  lesion  just  before  the 
onset  of  necrosis  and  caseation,  that  is,  they  appear  to  be 
mainly  made  up  of  the  so-called  epithelioid  cells,  with  occa- 
sionally a  well  formed  giant  cell.  Sometimes  the  outlines  of 
these  epithelioid  cells  are  distinct,  but,  as  a  rule,  wherever  the 
bacilli  are  numerous  there  appears  to  have  been  a  partial  fusion 
of  the  cell  bodies,  and  the  appearance  is  that  of  a  sort  of  matrix 
substance  with  imbedded  nuclei.  The  majority  of  these 
nuclei  are  vesicular  but  shrivelled  or  distorted  in  appearance, 
and  they  stain  lightly  as  compared  with  anj^  of  the  nuclei  in 
the  surrounding  normal  tissue.  According  to  M'Fadyean, 
the  important  points  to  notice  are  that  the  diseased  tissue  is 
never  sharply  delimited  and  that  there  is  no  actual  necrosis, 
although  the  appearance  of  the  new  tissue  may  be  interpreted 
as  indicating  that  the  cells  are  on  the  point  of  losing  their 
vitality.  Within  the  parts  which  contain  large  numbers  of 
bacilli  there  are  also  sometimes  recognizable  small  round  com- 
pact nuclei,  apparently  belonging  to  cells  of  the  lymphocyte 
type,  and  at  their  margins  there  are  numerous  cells  whose 
bodies  stain  red  with  Pappenheim's  stain. 

The  bacilli  do  not  appear  to  be  specially  intra-cellular  ; 
many  of  them  seem  to  be  lying  free,  and  others  appear  to  be 


PREVENTION  233 

situated  within  the  fine  reticulum  of  the  villi.  The  structural 
alterations  are  everywhere  proportional  to  the  number  of 
bacilli,  which  indicates  that,  contrary  to  what  is  the  case  in 
tuberculosis,  the  bacilli  have  little  or  no  tendency  to  degener- 
ate and  disappear  from  the  older  lesions.  The  bacilli  when 
numerous  are  generally  arranged  in  clumps  or  groups,  and 
these  often  form  a  very  large  part  of  the  epithelioid  areas. 

The  lesions  in  the  lymphatic  glands  have  a  similar  his- 
tology. They  may  be  present  either  in  the  cortex  or  the 
medulla,  but  they  are  not  tuberculous  in  the  anatomical  sense. 
A  small  number  of  giant  cells  may  be  present. 

The  course  of  the  disease  varies  from  a  few  weeks  to 
several  months.     It  seems  to  be  fatal  in  most  cases. 

§  163.  Differential  diagnosis.  This  affection  is  to  be 
differentiated  from  tuberculosis  and  parasitic  enteritis.  The 
non-virulence  of  the  organism  for  guinea  pigs  is  the  most 
reliable  differential  test  between  it  and  the  bovine  tubercle 
bacteria  The  finding  of  these  acid- fast  bacteria  and  the 
absence  of  distinct  lesions  and  parasites  would  distinguish  it 
from  the  other.  As  this  disease  is  liable  to  occur  in  conjunc- 
tion with  genuine  tuberculosis,  great  care  must  be  exercised 
in  making  the  diagnosis.  In  some  of  these  cases  reported 
there  appears  to  have  been  such  a  mixed  infection. 

§  164.  Prevention.  Johne's  disease  must  be  regarded  as 
one  which  results  from  infection  and  from  infection  only. 
M'Fadyean  states  that  in  all  the  cases  which  have  come  under 
his  observation  there  was  a  history  of  similar  cases  on  the 
farm  in  several  instances  extending  back  over  a  period  of 
many  years.  During  the  advanced  stages  of  the  disease  large 
numbers  of  the  bacilli  must  be  voided  with  the  feces,  and  m 
all  ordinary  circumstances  there  are  ample  opportunities  tor 
infection  from  this  source.  In  this  way  both  pasture  and 
other  materials  as  well  as  drinking  water  may  become  seriously 
contaminated.  At  the  present  moment  there  is  no  knowledge 
with  regard  to  the  resistance  of  the  bacilli  outside  the  body. 


234  OVINE    CASEOUS    LYMPH-ADENITIS 

or  the  length   of  time   that  a  contaminated    pasture    may    be 
dangerous. 

In  the  present  state  of  knowledge  the  question  of  preven- 
tion is  an  extremely  difficult  one  in  the  case  of  farms  on  which 
the  disease  has  existed  for  a  number  of  years.  The  isolation  or 
destruction  of  diseased  and  suspected  animals  should  be  prac- 
ticed. If  in  stables  the  feces  passed  by  diseased  or  suspected 
animals  ought  to  be  burned.  Cattle  should  be  kept  off  from 
pastures  in  which  such  animals  have  run.  As  the  time  during 
which  the  bacteria  remain  alive  outside  of  the  body  is  not 
known,  it  is  impossible  to  indicate  the  period  during  which 
infected  pastures  are  dangerous  to  other  cattle. 

REFERENCES. 

1.  Bang.  Chronische  pseudotuberculose  Darmentziindung  beim 
Rinde.     Berliner  TieriirzUiche  Wochenschrift,  1906,  p.  759. 

2.  BORGEAUD.     Schweizer  Archiv.  f.  Tierheilk.,  (1905),  p.  221. 

3.  JOHNE  AND  FroThixgham.  Ein  eigenthiimlicher  Fall  von 
Tuberkulose  beim  Rind.  Zeitschrijt  fur  Thiermedicin,  Vol.  XXI 
(1894),  p.  438. 

4.  LiENAUX  AND  EeckhouT.  Contribution  a  1'  ^tude  d'une 
entente  tuberculeuse  speciale  et  de  la  diarrhee  chronique  du  boeuf. 
Aniiales  de  Medecine  Veterinaire,  Vol.  LIV  (1905),  p.  65. 

5.  Markus.     Zeitsch.f.  Tiermediciv ,  Bd.  VIII  (1904),  P-  68. 

b.  M'Fadyean.  Johne's  disease  ;  a  chronic  bacterial  enteritis  of 
cattle.    Jour,  of  Compar.  Path,  atid  Thera.,  Vol.  XX  (1907),  p.  48. 


OVINE  CASEOUS  I.YMPH-ADEXITIS    (PSEUDO-TUBERCULOSIS 
IN  SHEEP). 

Synonyms.      Pseudo-tuberculosis  ;  ca.seous  adenitis. 

§  165.  Characterization.  Caseous  lymph-adenitis  is  a 
disease  of  adult  sheep  which  until  recently  was  designated  as 
pseudo-tuberculosis.  It  has  been  characterized  by  an  enlarge- 
ment of  one  or  more  lymphatic  glands,  which  contain  foci  of  a 
greenish-yellow,  caseous  or  purulent  substance.  It  is  rarely 
found  in   young    animals.     The   mortality    is    very    low,    due 


ETIOLOGY 


235 


perhaps  to  the  fact  that  the  sheep  are  slaughtered  before  the 
disease  has  time  to  develop.  It  does  not  occur  in  epizootic 
form  although  it  is  more  prevalent  in  certain  localities  than  in 
others. 

sj  166.  History.  The  name  "ovine  caseous  lymph 
adenitis"  was  proposed  by  Norgaard  and  Mohler  in  1899. 
These  writers  found  the  lesions  and  the  accompanying  micro- 
organism to  correspond  with  those  described  by  Preisz  and 
Guinard  in  1891  as  pseudo- tuberculosis.  The  bacterium  was 
fully  described  by  Preisz  in  1894.  The  organism  has  been 
found  and  identified  from  a  large  variety  of  lesions  in  a  number 
of  species  of  animals.  It  appears  that  at  least  many  of  the 
casesof  lymphatic  gland  enlargement  in  sheep  heretofore  called 
pseudo-tuberculosis  belong  to  this  disease.  Gilruth  prefers  the 
name  pseudo-tuberculosis.  Cherry  and  Bull  describe  it  as 
caseous  lymphatic  glands  and  Sivori  as  caseous  broncho-pneu- 
monia, the  bacterium  of  Preisz  being  found  as  the  probable 
cause  in  each  case. 

§  167.  Geographical  distribution.  In  the  United 
States  this  disease  is  quite  common  in  certain  districts  in  the 
western  and  southwestern  states.  It  exists  in  South  America, 
New  Zealand,  Australia  and  Europe. 

Sivori  found  that  10  per  cent  of  the  old  sheep  killed  in 
Buenos  Ay  res  were  affected.  The  prevalence  of  the  disease  in 
the  United  States  is  indicated  by  the  reports  of  the  federal 
meat  inspectors,  which  show  that  of  16,000,000  sheep  slaugh- 
tered in  Chicago,  Kansas  City  and  South  Omaha  3,236  were 
condemned  for  caseous  lymph-adenitis  or  lesions  which  might 
be  confounded  with  it.  It  is  reported  by  an  inspector  from  Los 
Angeles  that  of  950  sheep  coming  from  a  certain  district,  82 
were  suffering  from  lymph-adenitis. 

§  168.  Etiology.  Caseous  lymph-adenitis  is  caused  by 
a  specific  microorganism  first  described  by  Preisz  as  the 
bacillus  of  pseudo- tuberculosis.  Its  description  shows  it  to 
vary  in  size  to  such  a  degree  that  its  polymorphism  is  said  to 
be  characteristic.      It  is  non-motile  and  hence  belongs  to  the 


236 


OVINE    CASEOUS    LVMPH-ADEXITI5 


genus  Bacterium.  It  is  aerobic,  facultative  anaerobic,  stains 
readily  and  does  not  produce  spores.  It  develops  readily  on 
ao-ar  when  this  medium  is  inoculated  from  the  caseous  material 


Fig.  56.     Bacterium    of  Preisz.     Bacterium    in    pus    cells    1-12    obj . 
4   ocular    [Gilruth). 

from  the  affected  glands.  It  is  pathogenic  for  mice,  guinea 
pigs  and  rabbits.  The  organism  isolated  by  Gilruth  seems  to 
have  been  more  virulent  than  the  one  isolated  by  Xorgaard 
and  Mohler. 

§  169.  Symptoms.  In  the  majority  of  cases  no  symp- 
toms of  any  importance  are  observed  in  the  affected  animals 
during  life.  The  course  of  the  disease  is  that  of  a  chronic 
affection  and  the  pathological  changes  develop  so  slowly  that 
no  general  or  local  interference  with  the  health  of  the  affected 
animals  is  observed  in  lambs  and  sheep  that  are  bred  and 
raised  for  mutton  and  are  marketed  before  they  are  two  years 
old.  Only  in  breeding  ewes  and  wethers  does  the  disease 
advance  to  a  degree  which  makes  it  clinically  recognizable 
without  the  aid  of  manipulation.       The  affected  animals  upon 


SYMPTOMS  237 

examination    show    an    enlargement    of  one    or    more    ot    the 
superficial  glands,  the  precrural   and   the   sub-scapular   glands 
being  most  often  involved.     The  animals  thus  affected   appear 
in  every  other  respect  to  be  in   perfect   health.     In   the  older 
animals,  the  wethers  and  breeding  ewes,  the  same  glands  may 
be  enlarged  to  a  considerable  degree,  reaching   the  size  of  a 
hen's  egg  or  even  larger.     Some  of  these  sheep  may  show  a 
certain   degree   of    unthriftiness   or   even    emaciation.        The 
disease  is  found  in  its  most  advanced  stages  in  the  older  ewes, 
which  is  probably  due  to  the  fact  that  the  wethers  are  gener- 
ally disposed  of  before  they  are  three  years  old,  while  a  good 
breeding  ewe  is  frequently  retained  for  seven  or  eight  years. 
In  such  old  animals  the  superficial  lymphatic  glands  may  be 
enlarged   to  such  a   degree  as  to   interfere   with    locomotion, 
while  the  deeper  seated  glands  and  those  of  the  body  cavities 
are  similarly  affected.     In  the  advanced  cases  the  lesions  often 
become  disseminated  by  metastasis  to  the  principal  organs  of 
the  body.     In  such  cases  the  disease  may  assume  the  appear- 
ance of   chronic  broncho-pneumonia  or    pleurisy,   with    occa- 
sional cough,  slight  dyspnea  and  increasing  emaciation    and 
anemia.     The  course  of  the  disease  is  exceedingly  slow.     For 
this  reason  owners  of  affected  flocks  are  often  totally  ignorant 
of  the  presence  of  the  disease.     This  fact  renders  it  very  diffi- 
cult to  obtain  reliable    information    regarding    its   prevalence 
save  from  the  statistics  obtained  from    the  slaughter  houses. 
A  majority  of  the  inspectors  have  until  recently  classified  the 
lesions    either    as    tuberculosis,    pyemia    or    abscesses.       In 
response  to  inquiries  it  was   found  that  the   majority  of  cases 
which    had    been    condemned    under    these    headings    were 
undoubtedly  caseous  lymph-adenitis.     Several  thousand  cases 
are  annually  observed  in  the  slaughter  houses  of  the  United 
States,  but  only  a  fraction  of  these  are   advanced  to   a  degree 
that  would  warrant  a    total  condemnation    of    the   carcasses. 
Meat  inspectors  agree  that  lambs  are  very  rarely  aflfected,  and 
that  the  progress  of  the  morbid  changes  in  the  majority  of 
cases  is  coordinate  with  the  age  of  the  animal. 


238  OVIXE    CASEOUS    LYMPH-ADENITIS 

§  170.  Morbid  anatomy.  The  principal  lesions  are 
confined,  according  to  the  various  descriptions,  especiallj'  that 
by  Norgaard  and  Mohler,  to  the  lymphatic  glands.  In  many 
cases  only  a  single  gland  is  affected.  The  relative  frequency 
with  which  the  various  glands  become  the  seat   of  the  lesions 


Fig.  57.     The  leg  of  a  rabbit  slio-unng  enlarged  glands  after  inoculation 
Ti'itli  the  Bacterium  of  Preisz  {Norgaard  and  Mohler). 

may  be  given  as  follows  :  prescapular,  precrural,  superficial 
inguinal,  bronchial,  mediastinal,  sub-lumbar,  deep  inguinal, 
and  scrotal.  Rarely  the  suprasternal  and  mesenteric  glands 
are  affected.  Sivori  mentions  the  mesenteric  glands  among 
those  frequently  affected.  He  fails,  however,  to  mention  the 
mesenteric  glands  as  the  seat  of  lesions  in  the  detailed  descrip- 
tion of  twelve  typical  cases  of  caseous  broncho  pneumonia 
caused  by  the  bacillus  of  Preisz. 

When  first  invaded  by  the  bacterium,  the  adenoid  tissue 
becomes  hyperplastic  and  the  gland  enlarges  to  several  times 
its  original  size.  On  section  the  surface  is  found  to  be  watery, 
but  otherwise  the  tissue  retains  its  normal  appearance.  This 
is  followed  by  the  formation  of  various  centers  of  degeneration 
which  show  concentric  layers  and  gradually  become  confluent. 
Finally,  the  total  volume  of  the  gland  is  transformed  into  a 
homogeneous,  caseous  mass.  At  the  same  time  the  distended 
capsule  increases  in  thickness  and  forms  a  sac  which  confines 
the  semifluid,  grumous  inass.  In  rare  instances  the  sac  rup- 
tures and  when  close  to  the  surface  the  contents  will  be  dis- 
charged.    Under  ordinary  circumstances,  the  caseous  contents 


MORBID    AXATO:\IV  239 

become  cohesive  and  sticky  and  of  the  consistency  of  putty. 
In  very  old  cases  the  mass  becomes  dry  and  mealy,  with  little 
or  no  tendency  to  calcification.  The  greenish  yellow  color  oi 
the  caseous  mass,  which  is  stated  to  be  most  characteristic, 
closely  resembles  the  contents  of  the  intestinal  nodules  pro- 
duced by  Oesophagostoma  Cohimbiaimtti.  In  very  advanced 
cases,  as  for  instance  those  of  old  breeding  ewes,    the   internal 


) 


^        ' 

Fig.  58.     Lung  of  sheep  studded  with  nodules  [Gilruth] . 

organs  may  contain  lesions  which  microscopically  resemble 
those  of  tuberculosis.  The  lungs  may  be  studded  with  small 
nodulesthesizeof  a  pea,  the  spleen,  liver  and  in  rare  instances 
the  kidneys  also  may  contain  one  or  more  foci  of  the  same 
character,  namely,  a  mass  of  greenish  yellow  material,  sur- 
rounded by  a  firm,  fibrous  wall.  There  seems,  however,  to  be 
a  distinct  line  of  demarcation  between  the  affected  and  the 
healthy  tissue.  The  bronchial  and  the  mediastinal  glands 
may  be  affected  to  a  considerable  extent  without  any  lesions 
being  found  in  the  lungs.  In  some  cases  the  lungs  are  ex- 
tensively involved.  The  lesions  consist  of  nodules  varying  in 
size  from  that  of  a  millet  seed  to  that  of  a  walnut.  This  con- 
dition is,  as  a  rule,  accompanied  by    a   chronic   pleurisy    with 


240  OVINE    CASEOUS    LYMPH-ADENITIS 

extensive  adhesions  and  also  effusions  into  the  pleural  cavities. 

In  the  liver  the  lesions  consist  largely  of  nodules  com- 
posed like  those  in  the  lymphatic  glands,  of  a  firm  white 
fibrous  sac  containing  a  greenish-yellow,  cheesy  mass  of  vary- 
ing consistency.  Cases  have  been  reported,  however,  where 
the  entire  organ  was  filled  with  miliary  nodules. 

The  kidnej^s  are  rarely  affected,  but  when  they  are  the 
lesions  assume  the  same  characteristic  appearance  of  a  firm 
walled  abscess  protruding  on  the  surface  of  the  organ.  As  a 
rule,  only  one  or  two  such  foci  are  observed  in  each  case. 

A  histological  examination  of  tissues  containing  miliary  or 
sub-miliary  nodules,  shows  them  to  be  composed  chiefly  of 
leucocytes  and  nucleated  round  cells,  the  greater  part  of  which 
are  irregular  in  shape,  especially  toward  the  center  where 
many  of  them  are  transformed  into  a  granular  detritus. 
Among  the  cells  arranged  singly  or  in  clumps,  are  seen  the 
short  bacteria  which  stain  irregularly.  The  shape  varies  con- 
siderably from  oval  or  oblong  to  a  dumb-bell  shape. 

The  bacteria  are  frequently  seen  within  the  degenerated 
leucocytes,  the  destruction  of  which  is  due,  according  to 
Preisz,  to  the  specific  chemical  products  elaborated  by  these 
microorganisms. 

The  microscopic  appearance  is  somewhat  similar  in  all  the 
lesions  whether  located  in  the  lymph  glands,  lungs,  liver,  kid- 
neys or  spleen.  In  the  lungs  the  histological  picture  resem- 
bles that  of  broncho-pneumonia.  In  the  liver  the  lesions 
originate  in  the  portal  capillaries,  where  the  bacteria  cause  a 
proliferation  of  the  endothelial  cells,  which,  together  with  the 
accumulation  of  leucocytes  and  red  corpuscles,  cause  the  obli- 
teration of  the  vessels.  In  no  case  have  giant  cells  been  ob- 
served. The  surrounding  hepatic  cells  become  swollen,  then 
granular,  and  finally  they  undergo  atrophy,  leaving  open 
spaces  between  them.  Numerous  round  cells  appear  in  the 
periphery  of  the  nodules,  which  gradually  undergo  a  connec- 
tive tissue  metamorphosis  and  become  organized  into  an  en- 
capsulating membrane. 

When  a  miliary  nodule  from  the  liver  of  an  experimental 


MORBID    ANATOMY  24! 

animal,  which  has  been  destroyed  three  weeks  after  inoculation, 
is  examined  microsopically  the  following  picture  is  observed  : 
A  caseous  center  composed  of  an  amorphous  material  that  does 
not  take  any  of  the  ordinary  stains.  Surrounding  the  center 
may  be  seen  numerous  leucocytes  more  or  less  degenerated  and 
frequently  containing  one  or  more  bacteria,  while  clumps  of 
these  organisms  are  scattered  among  them.  External  to  this 
is  a  dense  round  cell  infiltration,  the  peripheral  zone  of  which 
is  undergoing  connective-tissue  formation,  thus  serving  as  a 
line  of  demarcation  between  the  atrophied  liver  cells  and  the 
central  cell  mass.  The  process  then  repeats  itself  until  a  con- 
nective-tissue barrier  strong  enough  to  encapsulate  the  central 
part  of  the  nodule  and  prevent  its  further  growth  is  obtained. 
The  nodules  in  the  kidneys  and  lungs  present  a  similar  micros- 
copic appearance,  excepting  that  the  foci  in  the  lungs  are  more 
regular  on  account  of  the  catarrhal  inflammation  that  accom- 
panies the  reaction  of  the  surrounding  tissue.  The  center  con- 
tains a  dense  mass  of  disintegrated  cell  structures  composed  of 
the  desquamated  and  proliferated  epithelial  cells,  degenerated 
leucocytes  and  round  cells.  In  experimental  animals  which 
succumb  quickly  to  an  intravenous  injection  of  virulent  ma- 
terial, the  lung  tissue  immediately  surrounding  the  nodules  is 
frequently  seen  to  be  hepatized. 

According  to  Gilruth  the  lesion  commences  by  the  arrest 
of  the  specific  bacterium  generally  in  a  lymph-gland  where  one 
or  more  are  surrou'nded  by  and  included  within  the  phagocytes. 
The  micro-organisms  multiply  within  the  cell  and  ultimately 
cause  the  degeneration  and  death  of  the  latter.  Simultane- 
ously a  slow  chronic  inflammation  occurs  around  the  focus  of 
attack  ;  there  is  proliferation  of  connective  tissue-cells  and  the 
formation  of  more  or  less  new  fibrous  tissue.  As  the  process 
spreads  outwardly  the  centre  degenerates,  and  the  protecting 
wall  increases  in  thickness.  In  fact,  all  the  phenomena  of  the 
pathology  of  true  tuberculosis  in  a  gland  occurs,  with  the  ex- 
ception of  the  formation  of  giant  cells.  The  degenerated  centre 
of  the  nodule  assumes  a  greenish  tint,  especially  distinct  at  the 
time  of  exposure  by  the  knife,  but  becoming  gradually  grayer 


242 


OVINE    LYMPH-ADENITIS 


afterwards.  In  the  centre  of  the  older  purulent  or  caseous 
mass  (for  the  consistence  varies  from  that  of  cream  to  that  of 
cheese  in  different  tumours)  there  are  usually  present  no  bacilli 
which  can  be  demonstrated  by  the  microscope  or  by  cultural 
methods. 

§  171.  Differential  diagnosis.  This  specific  lymphatic 
affection  is  to  be  differentiated  from  : 

1.  Infections  of  various  kinds,  not  recognized  as  specific, 
which  may  cause  enlargement  or  suppuration  of  lymph  glands. 

2.  The  specific  infectious  diseases,  such  as  tuberculosis. 

3.  Lymphadenoma. 

If  the  diagnosis  cannot  be  made  from  the  gross  appear- 
ance of  the  lesions  a  bacteriological  examination  will  be  neces- 
sary. The  fact  should  be  kept  in  mind  that  tuberculosis  in 
sheep  is  very  rare.  In  lymphadenitis,  cultures  in  ordinary 
media  will  give  a  growth  of  the  bacterium  of  Preisz.  With 
tuberculosis  the  results  would  be  negative  (see  tuberculosis). 
It  is  important  not  to  confuse  the  nodular  disease  of  .sheep's 
intestines  with  this  affection.  The  location  of  the  lesions  in 
the  walls  of  the  intestine  will  be  quite  sufficient  to  determine 
the  nodular  disease. 

REFERENCES. 

1.  Cherry  AND  Bull.  Caseous  lymphatic  glands  (pseudo -tuber 
culosis)  in  sheep.      The  Veterinarian,  Vol.  LXXII,  p.  523. 

2.  EberTH.  Bacillare  Nekrose  der  Leber.  Virchow's  Archiv, 
Bd.  C  (1885),  p.  23. 

3.  GiLRUTH.  Pseudotuberculosis  in  sheep.  (Lymphadenitis). 
Jour.  Compar.  Path,  and  Thera.,  Vol.  XV  (1902),  p.  324. 

4.  GiLRUTH.  Pseudo-tuberculosis  in  sheep.  (Lympho-adenitis). 
Bulletin  No.  i,  New  Zealand  Dept.  of  Agriculture. 

5.  NoRGAARD  AND  MoHLER.  The  nature,  cause,  and  economic 
importance  of  ovine  caseous  lymph-adenitis.  Sixteenth  Annual 
Report,  Bureau  of  Animal  Industry,  1899,  p.  638.    (Full  bibliography). 

6.  Preisz  AND  Guinard.  Pseudo-tuberculose  chez  le  mouton. 
Jour,  de  mi'd.  de  vH.  et  de  zootech,  ser.  3,  Vol.  XVI  (1891),  p.  563. 

7.  Preisz.     Recherches  comparatives  sur   les   pseudotuberculoses 


SVMl'TOMS  243 

bacillaires  et  une  nouvelle  espece  de  pseudotuberctilose.     ^hm.  de  l' Inst. 
Pasteur,  Vol.  VIII  (1894),  p.  231. 

8.  vSivoRi.  Sur  une  broncho-pneumonie  caseouse  du  mouton, 
causee  par  le  bacille  de  Nocard-Preisz.  Rev.  de  mi'd.  vet.  ser.  8,  Vol. 
VI  (1899),  p.  657. 


ASTHENIA  IN  FOWLS  AND  PIGEONS 

§  172.  Characterization.  This  is  a  disease  especially 
of  chickens  and  pigeons  in  which  there  is  marked  emaciation 
and  a  failure  to  take  on  flesh  even  when  fed  on  the  most 
nourishing  food.  Because  of  this,  the  disease  has  received  the 
popular  name  of  "  going  light." 

I  173.  History.  Although  this  condition  or  disease  has 
been  recognized  for  a  long  time,  it  seems  to  have  been  first 
described  in  1898  by  Dawson.  He  gives  a  brief  account  of  the 
symptoms,  morbid  anatomy,  etiology  and  a  somewhat 
extended  description  of  the  specific  organism  which  he  isolated 
from  the  diseased  chickens.  The  writer  has  studied  this 
affection  in  pigeons  but  did  not  succeed  in  finding  the  organ- 
ism isolated  by  Dawson. 

§  174.  Etiology.  Dawson  found  this  disease  to  be  due 
to  the  presence  of  a  certain  species  of  bacterium  which  he 
obtained  in  pure  culture  from  the  duodenal  contents.  He 
described  it  as  Baderhim  asthenice.  This  organism  varies 
from  I  to  1.3//  in  length  and  about  0.5//  in  width  with  rounded 
ends.  It  is  reported  to  possess  the  peculiarity  of  vegetating 
in  temperatures  varying  from  50  to  120°  F.  It  is  fatal  to  rab- 
bits within  24  hours  when  inoculated  into  the  abdominal 
cavity  with  0.5  c.  c.  of  a  bouillon  culture.  Chickens  inocu 
lated  with  this  organism  remained  well. 

§  175.  Symptoms.  The  only  symptoms  which  seem  to 
be  in  evidence  are  the  gradual  loss  of  flesh  and  an  exceedingly 
good  appetite.  It  is  reported  by  certain  pigeon  fanciers  con- 
cerning pigeons  and  the  fact  is  reiterated  by  Dawson,  that  the 


244  MISCELLANEOUS    INFECTIONS 

disease  is  an  exceedingly  chronic  one,  often  extending  over  a 
period  of  several  months  but  usually  terminating  in  death. 
In  the  cases  reported,  the  fowls  were  well  kept  and  given  an 
abundance  of  nourishing  food.  There  seems  to  be  an  inability 
on  the  part  of  the  affected  animal  to  assimilate  nourishment. 

§  176.  Morbid  anatomy.  The  most  conspicuous  lesion 
is  extreme  emaciation.  According  to  Dawson  the  mucosa  of 
the  duodenum  contains  areas  in  which  the  walls  are  deeply 
reddened  and  in  which  the  contents  are  of  a  mucoid  substance. 
The  writer  made  a  number  of  post-mortems  in  pigeons  suffer- 
ing from  this  disease  without  finding  any  gross  tissue  changes. 

The  disease  needs  further  investigation,  but  the  fact  that 
an  organism  has  been  found  in  the  duodenum  in  large  numbers, 
where  it  multiplies  and  apparently  produces  by-products  that 
are  absorbed  and  which  interfere  with  the  normal  metabolism 
of  the  body,  is  of  sufficient  interest  to  call  attention  to  the  pre- 
liminary findings  herein  mentioned.  It  is  not  unlikely  that  if 
the  present  hypothesis  concerning  the  nature  of  this  disease  is 
verified,  a  numberof  disorders  now  attributed  to  general  causes 
may  be  traced  to  some  form  of  intestinal  infection. 

REFERENCES 

I.  Dawson.  Asthenia  (going  light)  in  fowls.  Annual  Report 
of  the  Bureau  of  Animal  Industry,  U.  S.  Department  of  Agriculture, 
1898,  p.  329. 


MISCELLANEOUS  INFECTIONS 

§  177.  Diphtheria  in  calves  and  swine.  Diphtheria 
of  calves  is  an  infectious  disease  of  young  calves  characterized 
by  the  formation  of  a  diphtheritic  membrane  (necrosis)  on  a 
greater  or  less  portion  of  the  mucous  membrane  of  the  mouth 
and  throat.  It  often  leads  to  septicemia  and  death.  It  is 
caused  by  the  Bacterium  of  necrosis,  described  by  Bang. 

The  affection  is  quite  common  in  Europe  but  it  does  not 
seem  to  be  as  well  known  in  this  country. 


MISCELLANEOUS    INFECTIONS 


^45 


Loeffler,  who  investigated  diphtheria  of  calves  for  the 
German  Imperial  Board  of  Health,  believes  that  the  specific 
cause  of  the  disease  is  a  bacillus,  and  not  a  micrococcus,  as 
Daramann  assumed.  He  found  on  the  edges  of  the  necrotic 
tissue  large  long  bacteria  which  formed  undulating  threads, 
and  which  differed  entirel}^  from  the  bacterium  of  diphtheria  of 
man.  Ritter  confirmed  the  observations  of  Loeffler.  On  the 
other  hand,  Kitt  regards  the  cause  of  diphtheria  of  calves  to 
be  the  bacillus  of  necrosis. 

Swine  suffer  from  a  diphtheritic  necrosis  of  the  upper  por- 
tions of  the  digestive  canal  and  air  passages.  Johne  seems  to 
have  been  the  first  to  point  out  the  diphtheritic  character  of 
this  necrosis.  He  was  not  able  to  demonstrate  its  cause 
although  the  bacillus  of  necrosis  was  found  on  the  mucous 
membranes.  Swine  suffering  from  hog  cholera  frequentlj^  have 
areas  of  necrosis  in  the  gums,  tongue  and  other  parts  of  the 
mouth. 

Kitt  believes  that  there  occurs  sporadically  an  independent 
diphtheria  of  pigs  which  has  no  connection  with  swine  fever. 
He  believes  its  cause  is  the  bacillus  of  necrosis,  which  occurs 
also  in  diphtheria  in  calves.  The  mucous  membrane  of  the 
tongue,  cheeks,  phar3-nx  and  stomach  shows  yellow-white 
caseous  deposits  ;  and  that  of  the  small  intestine  and  colon, 
diphtheritic  necrosis. 

The  bacterium  (bacillus)  of  necrosis  has  been  found  to  be 
pathogenic  for  many  species  of  animals.  Mohler  {Pro.  Am. 
Vet.  Med.  Asso.,  1905,  p.  181)  has  pointed  out  the  extent  of  the 
pathological  activities  of  this  organism  in  cattle,  sheep,  goats, 
antelope,  several  varieties  of  deer,  horses,  asses,  hogs,  kan- 
garoos, dogs,  chickens,  pigeons,  rabbits,  guinea  pigs  and  mice. 
The  extent  and  variety  of  the  lesions  it  produces  have  sug- 
gested the  term  necrobacillosis  for  the  lesions  it  initiates. 


CHAPTER  VI. 


DISEASES  CAUSED  BY  BACTERIA 
GENUS  BACILLUS 


§  178.  General  discussion  of  the  genus  bacillus. 
The  genus  Bacillus  in  Migula's  classification  includes  all  rod- 
shaped  ynotile  bacteria.  In  the  older  classifications  it  includes 
both  non- motile  and  motile  forms.  The  fixing  upon  motility 
as  an  essential  generic  character,  and  thus  restricting  the 
genus  Bacillus  to  motile  forms,  is  the  occasion  of  some  con- 
fusion between  the  genera  Bacterium  and  Bacillus  as  applied 
to  a  number  of  important  disease-producing  bacteria.  It  is 
customary  to  speak  of  the  Bacillus  of  anthrax,  of  tuberculosis 
and  of  glanders  rather  than  of  the  Bacteritivi  of  these  affections. 
As  in  the  genus  bacterium,  there  are  a  number  of  species  of 
bacilli  that  are  widely  separated  from  each  other.  The 
diseases  which  they  produce  give  very  different  pictures  both 
clinically  and  in  their  morbid  anatomy. 


HOG  CHOLERA 


Syyiotiyms.'^      Swine    fever  ;     pneumo-enteritis  ;     pig    ty- 
phoid ;   Svinpest. 

§  179.     Characterization.     The  distinguishing  features 
of  this  disease  are  a  continuous  fever,  ulceration  of  the  intes- 


*This  disease  is  known  popularly  by  a  large  number  of  names  and 
in  some  works  on  swine  diseases  many  of  them  are  employed.  The 
more  common  of  these  are  enteric  fever,  typhus  carbuncular  fever, 
carbuncular  gastro-enteritis,  carbuncular  typhus,  pig  distemper,  blue 
sick7iess,  blue  disease,  purples,  ted  soldier,  a>ithra.x  fever,  scarlatina, 
measles,  diphtheria  and  erysipelas.  Many  of  the  terms  appear  to  refer 
to  some  one  or  more  of  the  observed  symptoms  or  lesions. 


HISTORY  247 

tines,  and  more  or  less  discoloration  of  the  skin,   especially 
over  the  ventral  surface. 

>^  180.  History.  The  earliest  outbreak  in  this  countr\^ 
of  which  there  is  knowledge  of  a  disease  supposed  to  be  hog 
cholera,  occurred  in  the  state  of  Ohio  in  1833.  It  is  presumed 
that  it  was  brought  from  Europe  with  some  of  the  animals 
imported  from  there  for  breeding  purposes.  After  being  intro- 
duced, it  spread  at  first  slowly,  but  later  with  increasing 
rapidity  along  the  lines  of  commerce,  until  it  invaded  every 
part  of  this  country  where  swine  raising  had  become  an 
industry.  The  disease  was  investigated  and  very  carefully 
described  by  Dr.  C.  Sutton,  of  Aurora,  Ind.,  from  1850  to 
1858.  In  1861,  Dr.  Edwin  M.  Snow,  of  Providence,  R.  I., 
contributed  an  important  paper  on  this  disease  to  the  U.  S. 
Department  of  Agriculture.  In  1875,  Dr.  James  Law,  of 
Ithaca,  N.  Y., 'furnished  to  the  same  Department  a  valuable 
paper  setting  forth  the  symptoms  and  morbid  anatomy  of  this 
disease.  He  believed  it  to  be  contagious  although  the  specific 
organism  had  not  been  found.  The  U.  S.  Commissioner  of 
Agriculture  appointed  in  1878  nine  men  for  a  period  of  two 
months  each  to  investigate  the  disease  in  various  localities. 
In  their  report  the  symptoms  and  morbid  anatomy  formerly 
described  were  confirmed  and  two  additional  features  set 
forth.  Law  showed  that  it  was  transmissible  by  inoculation  to 
other  animals,  and  Dr.  Detmers  described  a  microorganism 
which  he  called  Bacillus  suis  and  which  he  believed  to  be  the 
specific  cause  of  the  trouble.  Later,  Detmers  described  his 
organism  as  a  micrococcus.  The  work  of  investigation  was 
continued  under  the  direction  of  the  Commissioner  of  Agricul- 
ture and  finally,  in  1885,  the  specific  organism  was  discovered 
by  Salmon  and  Smith,  who  described  its  essential  characters 
and  properties.  It  was  called  Bacterium  of  swine  plague. 
Since  that  time  the  disease  has  been  under  investigation  and 
the  Bureau  of  Animal  Industry  has  during  the  last  few  years 
been  actively  engaged  in  the  efforts  to  produce  a  specific, 
therapeutic  serum. 

In  1886,  Dr.  Theobald  Smith  discovered  another  bacterial 


240  HOG    CHOLERA 

disease  among  swine.  It  was  found  to  be  similar  to  the 
German  Schzveineseuche ho\.\i  in  the  morbid  anatomy  and  in 
the  morphology  and  properties  of  its  specific  organism.  In 
naming  this  disease  the  Bureau  of  Animal  Industry  called  it, 
on  account  of  its  similarity  to  the  German  Sc/i-weiyieseiic/ic, 
swine  plague  and  its  organism  the  bacillus  of  swine  plague, 
and  changed  the  name  of  the  disease  described  in  1885  to  hog 
cholera  and  its  organism  to  the  bacterium"-^  of  hog  cholera. 
The  changing  of  the  name  of  the  first  disease  described  from 
swine  plague  to  hog  cholera  has  been  the  cause  of  some 
criticism  and  it  has  been  credited  with  the  responsibility  of 
creating  confusion.  It  has,  perhaps,  led  hasty  readers  to  a  mis- 
interpretation of  these  diseases  and  their  relation  to  those  de- 
scribed in  other  lands  under  different  names.  While  the  names 
assigned  may  not  have  been  especially  happy  ones,  the  trans- 
fer of  the  term  swine  plague  from  the  intestinal  to  the  lung 
disease  must  be  considered  as  a  fortunate  occurrence  and  one 
which  tended  to  simplify  and  not  to  confuse. 

Billings,  of  the  Nebraska  State  Experiment  Station, 
opposed  this  nomenclature.  He  not  only  refused  to  accept 
the  change  and  to  continue  to  write  about  hog  cholera  under 
the  title  of  swine  plague,  but  he  denied  the  existence  of  the 
swine  plague,  as  described  in  the  reports  of  the  Bureau  of 
Animal  Industry  for  1886  and  subsequently,  as  an  indepen- 
dent disease.  The  wide  dissemination  of  his  publications  on 
this  subject  has  unquestionably  been  responsible  for  much  of 
the  haziness  concerning  the  di.stinguishing  features  of  these 
maladies. 

In  1893,  Drs.  Welch  and  Clements  read  a  paper  before  the 
International  Veterinary  Congress  in  which  they  gave  a  very 
clear  history  of  the  nomenclature  of  these  diseases  and  in 
which  they  adhered  to  the  one  of  the  Bureau  of  Animal  In- 
dustry. 

§  181.     Geographical    distribution.      Hog    cholera    is 

*In  18SS  the   genus  Bacterium  was  changed   to  Bacillus   and   this 
organism  is  spoken  of  since  that  time  as  the  hog-cholera  bacillus. 


ETIOLOGY 


249 


widely  disseminated  throughout  the  central  part  of  the  United 
States.  It  exists,  however,  to  a  certain  degree  in  every  state 
in  the  Union  and  in  Canada.  It  has  long  been  known  in 
Great  Britain.  It  prevails  to  a  greater  or  less  extent  on  the 
continent  of  Europe.  The  confusion  that  has  arisen  in  the  use 
of  the  terms  swine  plague  and  hog  cholera  renders  it  difficult 
to  determine,  from  the  brief  description  given  in  a  number  of 
reports,  the  nature  of  the  disease  in  question. 

^  182.  Etiology.  The  specific  disease,  here  described  as 
hog  cholera,  is  caused  by  Bacillus  cholerae  suis/^  A  brief  des- 
cription of  its  morphology,  physiological  properties  and  patho- 
genesis are  appended. 


0,    .   •   ,  ' 


>;-• 


Fig.  59.     A  photoo:rapli  of  ihc  hacilliis  0/ /lo,^-  cholera  7vith   I  hi'  Jlagella 
slained.      X  aboiil  loon  diiunc/ers. 

*Moore  described  a  bacterium  found  in  a  pii;,  from  which  the  swine 
plague  organism  was  also  obtained,  that  possessed  the  cultural  and 
pathogenic  properties  of  the  hog-cholera  bacillus.  More  recenlly. 
Smith  has  described  a  similar  organism,  which  was  isolated  by  Burrell 
in  Illinois. 


250 


HOG    CHOLERA 


Morphology.— .\  rod-shaped  organism  varying  in  size  according  to 
the  medium  in  which  it  is  developed.  From  agar  cultures  it  is  from 
1.2  to  1.8//  long  and  from  .5  to  .8//  broad.     The  ends  are  rounded. 

Spores  have  not  been  observed.  It  is  actively  motile.  A  variable 
number  of  flagella  have  been  demonstrated  but  usually  there  are  from 
3  to  5.  The  length  of  the  flagella  varies.  The  average  seems  to  be 
about  7//  although  filaments  55//  with  an  average  length  of  35  to  40/;  are 
reported  by  Ferrier.  It  stains  readily  with  the  aniline  dyes.  Prepara- 
tions made  from  cultures  usually  stain  uniformly  ;  while  in  the  prepara- 
tions made  from  the  tissue  of  inoculated  animals  there  is  frequently 
exhibited  a  light  center  with  a  deeply  stained  periphery. 

Cultural  characters  and  biochcmic  properties. — The  bacillus  is 
grown  readily  on  all  of  the  ordinary  media  used  in  bacteriological  work 
at  a  temperature  of  30  to  38°  C.     It  is  aerobic  and  facultative  anaerobic. 

Agar.— On  the  surface  of  inclined  agar  after  24  hours  at  a  tempera- 
ture 37°  C.  a  grayish,  glistening  nonviscid  growth  appears.  When 
isolated  the  colonies  are  nearlj-  round,  convex,  0.5  to  2.0  mm.  in  diame- 
ter. The  edges  are  sharply  defined  and  even.  In  stab  cultures  a  grayish 
growth  develops  along  the  needle  track  with  a  more  vigorous  growth 
on  the  surface  about  the  needle  puncture.  The  growth  reaches  its  max- 
imum in  about  48  hours. 

Gelatin. — In  this  medium  the  growth  is  moderately  feeble,  the 
colonies  appearing  as  grayish  dots.  When  magnified  they  are  finely 
granular  and  of  a  yellowish  tint.  The  quantity  and  form  of  growth 
depend  considerably  upon  the  reaction  of  the  gelatin.  If  decidedly 
alkaline  there  is  often  a  tendency  for  the  growth  to  spread.  There  is  no 
softening  or  liquefaction  of  the  medium. 

Potato. — The  growth  on  potato  takes  the  form  of  a  very  thin,  glis- 
tening layer.  It  is  usuall}-  of  a  faintly  yellowish  color  but  this  is  sub- 
ject to  variation  on  different  potatoes.  If  the  reaction  is  strongly  acid 
no  growth  appears. 

Bouillon. — In  alkaline  bouillon  it  imparts  in  24  hours  a  uniformly 
cloudy  appearance  to  the  liquid.  Ordinarily  there  is  no  membrane  on 
the  surface.  After  some  days'  standing  the  growth  begins  to  settle, 
forming  a  grayish,  friable  sediment.  If  the  bouillon  contains  muscle 
sugar  the  reaction  will  be  changed  to  acid,  in  from  24  to  48  hours,  due 
to  the  fermentation  of  the  sugar.  Later,  however,  the  liquid  will 
become  strongly  alkaline,  unless  there  was  too  much  muscle  sugar 
present.  In  acid  bouillon  the  growth  is  less  vigorous.  It  grows  better 
in  a  bouillon  containing  peptone  than  in  a  simple  beef  broth. 

Milk. — When  the  milk  is  acid  in  the  beginning  it  gradually 
becomes  alkaline.  There  is  no  precipitation  or  coagulation  of  the 
casein,     .\fter  standing  for  from  two  to  three  weeks    in    an    incubator   a 


KTIOLOC.V  251 

gradually  developing  opalescence  of  the  milk  can  be  observed.  Later 
it  becomes  clear,  then  light  brownish  in  color.  If  allowed  to  stand 
longer  in  the  incubator  the  volume  of  the  culture  shrinks  by  evaporation 
and  the  opalescent  liquid  becomes  quite  thick  and  dark-colored  but  not 
viscid.  When  the  opalescence  appears  the  milk  is  strongly  alkaline. 
The  process  seems  to  be  a  form  of  saponification  of  the  fat  globules  due 
to  the  presence  of  the  alkali  produced  by  the  bacteria. 

I,uhil.  —  \n  Dunham's  solution  the  growth  is  quite  feeble.  Ordi- 
narily no  indol  reaction  is  obtained,  although  it  has  been  observed  in  a 
few  cultures  obtained  from  different  epizootics. 

Gas  production.— In  peptonized  bouillon  containing  i  per  cent 
dextrose,  gas  appears  within  24  hours  and  continues  to  form  for  from 
three  to  five  days.  During  the  first  day  from  one-fourth  to  one-half  of 
the  total  quantity  is  produced.  By  the  end  of  the  second  day  the  gas 
formation  is  nearly  at  an  end.  The  total  amount  which  collects  in  the 
closed  branch  of  the  fermentation  tube  is  equivalent  to  about  one-half 
of  the  capacity  of  this  branch.  The  gas  set  free  is  composed  of  CO._,  and 
an  explosive  gas  which  consists  largely  of  H.  The  ratio  of  CO.,  to  H  in 
the  fermentation  tube  is  approximately  as  1:2.  The  reaction  of  the 
liquid  becomes  strongly  acid,  which  condition  checks  the  multiplication 
of  the  bacteria. 

Gas  is  not  produced  in  bouillon  containing  lactose  or  saccharose. 
These  sugars  are  not  fermented.  Alkaline  cultures  containing  them 
become  more  strongly  alkaline  as  the  growth  continues. 

Thermal  reactions.— 1V\^  organism  grows  very  feebly  at  a  tempera- 
ture of  20°  C.  It  will  not  thrive  at  a  temperature  above  43°  C.  It  is 
destroyed  when  exposed  to  moist  heat  at  58^  C.  for  10  minutes. 

Disinfectants.— This  organism  is  destroyed  after  an  exposure  for  10 
minutes  or  less  in  the  following  solutions: 

Carbolic  acid,  i  per  cent.  Hydrochloric  acid,  1-5  of  i  per  cent. 
Sulphuric  acid,  1-20  of  i  per  cent.  Sulphate  of  copper,  1-4  of  i  per  cent. 
Formalin,  i  to  2,000.     Trikresol,  1-2  of  i  percent. 

Lime  is  also  a  good  disinfectant  when  used  in  preparations  contain- 
ing about  I  per  cent  CaO. 

Drying.— This  bacillus  resists  drying  for  a  variable  length  of  time, 
according  to  the  amount  of  protection  it  has.  In  a  drop  of  a  bouillon 
culture  dried  on  a  cover-glass  and  kept  under  bell  jars,  the  vitality  is 
retained  for  from  5  to  8  days.  In  bits  of  animal  tissue  containing  the 
bacilli,  the  vitality  is  retained  for  from  20  to  40  days,  according  to  the 
quantity  of  tissue  taken. 

Pathogenesis.— ^nhcvit&we^ous  injections  of  from  i  to  3  c.  c.  rarely 
produce  fatal  results  in  swine.  An  intravenous  inoculation  of  5  c.  c. 
usually  produces  a  septicemia.     With  smaller  doses  the  "button  ulcers" 


252  HOG    CHOLERA 

characteristic  of  hog  cholera  have  been  produced  (Welch).  By  feeding 
pigs  with  pure  bouillon  cultures  the  intestinal  lesions  typical  of  hog 
cholera  have  also  been  obtained  (Smith). 

Rabbits  inoculated  subcutaneously  with  o.i  c.  c.  of  a  bouillon  cul- 
ture die  in  from  5  to  8  days.  The  essential  lesions  consist  of  necrotic 
foci  in  the  liver  and  a  very  much  enlarged  and  dark  colored  spleen. 
Guinea  pigs  are  affected  similarly  to  rabbits,  but  death  does  not  usually 
occur  until  from  7  to  12  days.  Pure  cultures  of  the  bacillus  can  be 
obtained  from  the  blood,  liver  or  spleen  of  the  inoculated  animals. 

While  the  above  description  applies  to  the  form  most 
frequently  encountered,  varieties  are  not  uncon)mon.  In  1894 
Smith  called  attention  to  several  varieties  of  this  species.  It 
is  interesting  to  add,  that  Reed  and  Carroll  have  found  the 
bacillus  isolated  bj'  Sanarelli,  and  thought  by  him  to  be  the 
cause  of  yellow  fever,  to  belong  to  this  group  of  bacteria. 

In  1903,  de  Schweinitz  and  Dorset  published  the  discovery 
of  a  disease  practically  identical  in  its  manifestations  with  hog 
cholera  of  an  acute  type,  but  which  was  produced  by  a  virus 
that  passed  through  the  finest  porcelain  filters.  It  is  possible, 
therefore,  that  the  disease  now  known  as  hog  cholera  may  be 
differentiated  into  two  maladies,  one  caused  by  B.  cholerae  suis 
and  the  other  by  the  "invisible  virus  "  McClintock,  Boxraeyer 
and  Siffer  report  like  results  in  the  production  of  a  disease  with 
the  filtrate.  These  authors  were  unable  to  find  the  hog-cholera 
bacillus  in  the  cases  from  which  they  obtained  the  invisible 
virus.  This  suggests  that  they  are  dealing  with  a  new  disease 
rather  than  with  a  new  etiological  factor  for  hog  cholera. 
Until  this  infectious  filtrate  is  obtained  from  animals  from 
which  pure  cultures  of  B .  cholerae  suis  were  isolated  from  the 
organs,  it  seems  unfortunate  to  consider  it  the  cause  of  hog 
cholera.  The  experimental  results  obtained  with  ^.  cholerae  suis 
are  too  convincing  to  relegate  it,  without  sufficient  evidence,  to 
the  role  of  a  secondary  invader. 

More  recently  Dorset,  Bolton  and  McBryde  have  con- 
firmed the  earlier  publication  by  de  Schweinitz  relative  to  the 
filterable  virus.  They  state,  however,  that  "  it  must  be  ad- 
mitted that  a  disease  in  hogs  may  exist  which  is  due  to 
B.  cholerae  sjiis,  and  which  has  no  connection  with  the  filterable 


SVlNIP'rOMS 


253 


virus  found  by  us  in  the  outbreaks  we  have  studied."  They 
believe,  however,  that  such  a  disease  "  would  be  possessed  of 
a  low  degree  of  contagiousness." 

Tin  period  of  incubatiou  varies  from  7  to  14  days.  Berry 
states  that  it  varies  from  one  to  three  weeks  and  perhaps 
longer. 

§  183.  Symptoms.  The  symptoms  of  hog  cholera  are 
by  no  means  constant.  The  best  informed  writers  on  the  sub- 
ject agree  that  hog  cholera  can  not,  with  certain  exceptions, 
be  positively  diagnosed  from  the  symptoms.  Animals  suffering 
from  various  intestinal  troubles  frequently  exhibit  symptoms 
which  very  closely  resemble  those  of  this  disease. 

There  are  two  recognizable  forms,  namely,  the  acute,  and 
the  chronic  or  mild  form.  In  the  acute  disease,  the  animals 
die  very  suddenly  after  a  few  hours'  or  at  most  a  few  days' 
sickness.  In  the  other  form,  the  disease  runs  a  longer  course. 
There  is  usually  a  rise  of  temperature  of  from  i  to  3°  F. 

The  sick  animals  act  dumpish  and  spiritless  and  lie  quietly 
in  a  corner  or  huddle  together,  usually  concealing  the  head  in 
the  litter.  They  refuse  to  move  when  disturbed  and  are  more 
or  less  oblivious  to  their  suffering.  The  appetite  varies.  In 
acute  cases  the  animals  may  eat  quite  heartily  up  to  within  a 
few  hours  before  death.  In  more  chronic  forms  they  eat  fairly 
well  until  the  end.  There  may  or  may  not  be  diarrhea.  Fre- 
quently the  bowels  are  costive.  It  is  quite  common  in  these 
cases  to  have  an  active  diarrhea  during  the  last  few  days.  The 
color  of  the  discharge  depends  largely  on  the  food.  Vomiting 
rarely  occurs.  The  changes  in  the  respiration  and  the  pulse 
are  difficult  to  determine.  There  is  rarely  any  cough.  Usually 
there  is  considerable  reddening  of  the  skin  on  the  nose,  ears, 
abdomen  and  on  the  inside  of  the  thighs  and  public  region. 
Occasionally  this  reddening  is  very  marked.  The  redness  is 
diffuse  and  becomes  more  intense  as  death  approaches.  In 
some  cases  there  is  a  discharge  from  the  eyes.  In  the  chronic 
form  the  animal  becomes  emaciated.  These  symptoms  vary 
to  such  an   extent  that   it   is   .sometimes  necessary   to  make  a 


254 


HOG    CHOLERA 


post-mortem  examination  and  even  the  diagnosis  must  often 
be  delayed  until  the  results  of  a  bacteriological  examination 
have  been  obtained.  It  not  infre- 
quently happens  that  swine  suffering 
from  hog  cholera  are  attacked  with 
swine  plague,  the  two  diseases  co- 
existing in  the  same  animal. 

§  184.  Morbid  anatomy.  The 
acute  type.  This  might  with  equal 
propriety  be  called  the  hemorrhagic  or 
septicemic  type,  inasmuch  as  the  chief 
nd  perhaps  the  only  obvious  changes 
are  hemorrhagic  in  nature.  They  are 
more  con.spicuous  when  an  animal  is 
examined  immediately  after  death. 
The  spleen  is  variably  enlarged,  soft, 
and  gorged  with  blood.  Sometimes 
it  is  twice  as  long  as  normal  and  the 
other  dimensions  are  proportionately 
increased.  It  may  extend  across  the 
median  line  to  the  right  side.  Next 
to  the  spleen,  the  lymphatic  glands 
and  the  serous  membranes  are  most 
^ti^^  r  /V  severely  involved.  The  cortex  of  the 
glands  appears  on  section  as  a  hemor- 
rhagic line  or  band,  according  to  the 
amount  of  extravasated  blood,  or  the 
entire  gland  may  be  infiltrated  with  it. 
Among  the  glands  most  commonly 
hemorrhagic  are  those  of  the  meso- 
colon, those  at  the  root  of  the  lungs, 
and  on  the  posterior  thoracic  aorta. 
Besides  these,  the  retro-peritoneal  and 
the  gastric  glands  may  be  involved. 
More  rarely  the  mesenteric  glands  show  slight  blood  extrava- 
sations. Hemorrhages  are  also  quite  frequent  beneath  the 
serous  surfaces  of  the  abdomen  and  thorax.       They  are  most 


Fig.  60.  Ulcers  in  the  in- 
testine of  a  pig  dead  of 
hog  cholera. 


MORHID    ANATO-MV 


255 


abundant  as  petechiae  and  larger  patches  under  the  mucous 
membrane  of  the  large  and  small  intestines.  They  are  occa- 
sionally found  under  the  peri- 
toneum near  the  kidneys,  the 
diaphragm  and  the  costal  pleura 
as  extravasations  nearly  an  inch 
in  diameter. 

The  lungs,  in  a  small  per- 
centage of  cases,  show  subpleural 
ecchymoses  in  large  numbers 
and  on  section  small  hemor- 
rhagic foci  are  observed  through- 
out the  lung  tissue.  In  a  feu- 
cases  severe  hemorrhages  involv- 
ing one  or  more  lobes  have  been 
observed.  The  kidneys  are  oc- 
casionalh^  the  seat  of  extensive 
hemorrhagic  changes.  The 
glomeruli  appear  as  blood  red 
points;  larger  extravasations 
occur  in  the  medullary  substance 
and  blood  may  collect  around 
the  apices  of  the  papillae.  The 
subcutaneous  tissue  over  the 
ventral  surface  of  the  body  may 
be  dotted  with  petechiae  and  oc- 
casionally collections  of  blood 
(hematomata)  are  found  in  the 
superficial  muscular  tissue.  The 
brain  and  spinal  cord  have  not 
been  generally  examined.  In 
one  case,  petechiae  were  ob- 
served on  the  cerebellum. 

The  digestive  tract  usually 
is  the  seat  of  extensive  lesions. 
The  fundus  of  the  stomach  is  as  a  rule  deeply  reddened  ;  there 
may  be  more  or  less  hemorrhage  on  the  surface,  giving  rise  to 


Fig.  61.  Spleens  of  pigs  oj  thc 
same  age ;  {a)  dead  from  hog 
cholera,  [d)  normal  {killed  in 
health). 


256  HOG    CHOLERA 

larger  areas  of  blood  clots.  In  some  cases  the  small  intestine 
has  submucous  ecchymoses  throughout  its  entire  length.  In 
the  large  intestines  these  may  be  so  numerous  as  to  give  the 
membrane  a  dark  red  appearance.  The  intestinal  contents  are 
now  and  then  incased  in  a  layer  of  blood  clot. 

The  chronic  form  is  perhaps  the  most  common,  at  least  in 
those  epizootics  which  have  been  reported.  The  acute  hemor- 
rhagic cases  usually  die  in  the  beginning  of  the  outbreak  and 
are  apt  to  be  overlooked.  Following  these  are  the  more  pro- 
tracted ones.  In  these  animals  the  disease  may  be  limited  in 
its  manifestations  to  the  large  intestine,  although  the  other 
organs  are  not  exempt  from  degenerative  changes.  These  are 
due  in  part  to  the  impairment  of  the  functions  of  the  large 
intestine,  consequent  fermentations  and  the  absorption  of  the 
poisonous  products  elaborated  by  the  specific  bacilli  in  the 
spleen  and  other  organs. 

The  lesions  of  the  large  intestines  are  necrotic  and  ulcera- 
tive in  character.  The  ulcers  may  be  isolated  and  appear  as 
circular,  slightly  projecting  masses,  stained  yellowish  or 
blackish  or  both  in  alternate  rings,  or  they  may  be  slightly 
depressed  and  somewhat  ragged  in  outline.  When  the  super- 
ficial slough  is  scraped  away  many  ulcers  show  a  grayish  or 
white  base.  A  vertical  section  reveals  a  rather  firm  neoplastic 
growth,  extending  usually  to  the  inner  muscular  coat.  When 
sections  of  such  an  ulcer  are  stained  with  aniline  dyes  and  ex- 
amined under  the  microscope,  the  submucous  tissue  is  very 
much  thickened,  infiltrated  with  rounds  cells  and  containing  a 
large  number  of  dilated  vessels.  Resting  upon  this  thickened 
submucosa,  is  a  line  of  very  deeply  stained  amorphous  matter 
and  upon  this  is  situated  the  necrotic  mass  which  fails  to  retain 
the  coloring  matter  and  which  is  permeated  by  a  very  large 
number  of  bacteria  of  various  kinds.  Frequently  the  eggs  of 
trichocephalus  are  imbedded  in  the  slough. 

The  extent  of  the  submucous  infiltration  depends  upon 
the  age  of  the  ulcer.  In  old  ulcers  it  contains  many  newly- 
formed  capillaries,  and  evidences  of  the  formation  of  connective 
tissue  are  present.       The  capillaries  may    extend  to    the    very 


MORBID    ANATOMY  257 

edge  of  the  border  where  the  slough  begins.  The  latter  may 
have  been  parti}'  shed,  leaving  a  smooth  line  bounding  the 
cicatricial  tissue.  The  submucous  infiltration  gradually  disap- 
pears toward  the  periphery  of  the  ulcer  and  slightly  outside  of 
the  ulcer  no  inflammation  of  the  membrane  exists.  Giant  cells 
have  been  observed  in  the  intertubular  tissues  at  the  edge  of 
the  ulcer.  The  depth  to  which  the  infiltration  extends  is  not 
always  limited  to  the  submucosa  ;  it  may  extend  into  the 
muscular  coats  and  cause  inflammatory  thickening  and  in- 
flammation and  the  formation  of  new  vessels  in  the  subjacent 
serosa. 

In  some  cases  the  necrosis,  instead  of  appearing  in  circum- 
scribed ulcers  from  one-sixteenth  to  one-half  inch  or  more 
across,  involves  the  whole  surface  of  the  mucous  membrane, 
giving  it  the  appearance  of  a  so-called  diphtheritic  membrane. 
In  such  cases  the  walls  of  the  intestine  are  very  much  thick- 
ened and  so  friable  as  to  be  easily  torn  with  the  forceps  in 
handling  them.  Such  necroses  are  rare  in  epizootic  cases,  but 
they  frequently  appear  in  animals  which  have  been  fed  with 
pure  cultures  of  hog-cholera  bacilli. 

The  distribution  of  the  ulcers  varies  but  slightly.  The}' 
appear  most  frequently  in  the  cecum  and  on  the  ileo-cecal 
valve,  as  well  as  in  the  upper  half  of  the  colon.  The  lower 
half  is  implicated  in  severe  cases  only  and  then  less  extensively. 
The  rectum  is  rarely  ulcerated.  The  lower  portion  of  the 
ileum  is  ulcerated  in  a  small  percentage  of  animals,  especially 
when  they  have  been  fed  with  hog  cholera  viscera  or  cultures. 
The  stomach  is  occasionally  the  seat  of  slight  ulceration. 
The  lymphatic  glands  of  the  affected  intestine  are  usually 
much  enlarged,  pale,  tough  and  whitish  on  sections.  The 
spleen  is  rarely  enlarged.  The  liver  shows  degenerative 
changes.  The  heart  and  lungs  are  usually  normal.  The 
broncho-pneumonia  frequently  found  in  young  pigs  in  the 
winter  months  must  be  ascribed  priniaril\-  to  exposure  rather 
than  to  the  presence  of  hog  cholera. 

In  some  outbreaks  the  acute  and  the  chronic  types  are 
not  so  clearly   separated  as  indicated   in  the  foregoing  pages. 


258  HOG    CHOLERA 

Frequently  recent  hemorrhagic  lesions  seem  to  be  associated 
with  cases  presenting  extensive  ulcerations,  which  certainly 
are  much  older  than  the  extravasations.  It  may  be  that  the 
latter  are  the  result  of  a  secondary  invasion  of  the  hog-cholera 
virus,  either  from  the  ulcers  in  the  intestine  or  from  without. 
To  illustrate  more  fully  the  difference  in  the  lesions  of  the  two 
forms  of  the  disease,  the  published  post-mortem  notes  of  two 
cases  are  appended. 

(i)  Acute  fortn.  Female,  two  years  old,  weight  about  150  pounds. 
She  had  been  known  to  be  sick  but  a  few  hours.  The  examination  was 
made  two  hours  after  death.  A  little  blood  was  oozing  from  the  nostrils. 
The  skin  was  not  discolored.  Upon  section  the  skin  was  normal  in 
appearance.  The  liver  was  deeply  reddened,  due  to  engorgement  of  the 
blood  vessels.  Blood  flowed  freely  upon  section.  The  spleen  was 
slightly  enlarged  and  dark  colored  The  kidneys  were  hyperemic, 
especially  the  medullary  portion.  In  the  pelvis  of  the  right  kidney 
there  was  a  large  blood  clot.  The  mucous  membrane  of  the  intestines 
was  normal  with  the  exception  of  several  irregular  areas  of  hyperemia. 
In  the  fundus  of  the  stomach  was  a  large,  dark  blood  clot.  No  ulcers. 
The  mesenteric  glands  were  enlarged  and  darker  than  normal  In  a  few 
cases  the  cortex  was  hemorrhagic.  The  right  lung  was  in  a  state  of 
hyperemia.     The  heart  contained  very  little  liquid  blood. 

Bacteriological  examination. — A  few  bacteria  were  found  in  stained 
<;over-glass  preparations  from  the  spleen  aud  liver.  Tubes  of  slant  agar 
were  inoculated  with  bits  of  the  tissue  from  the  hyperemic  lung,  liver, 
spleen  and  kidneys.  These  tubes  developed  cultures  of  the  hog-cholera 
bacillus.  A  few  of  them  were  pure  cultures  ;  the  others  contained,  in 
addition  to  the  hog-cholera  organism,  a  quite  large  bacillus.  (Report 
N.  Y.  State  Com.  Agric.  1887). 

(2)  Chronic  form.  Small  female,  weight  about  20  pounds,  Con- 
siderable reddening  of  the  skin  over  the  ventral  aspect  of  the  body  and 
limbs  ;  especially  marked  along  the  median  line.  Superficial  inguinals 
enlarged,  of  a  mottled,  pale  and  deep  red  color  on  section.  Spleen 
very  large,  12  inches  long,  2  inches  broad,  and  five-eighths  to  three- 
fourths  inches  thick  at  the  hilus  ;  gorged  with  blood,  friable.  A  small 
number  of  punctiform  hemorrhages  in  cortical  portion  of  the  kidneys. 
Glands  of  mesentery  and  colon  enlarged  and  congested.  Deep  redden- 
ing of  several  square  inches  of  mucosa  fundus  of  stomach.  Large  intes- 
tine contains  a  semi-liquid  mass  chiefly  earth.  Four  large  ulcers  in  the 
cecum,  one  of  them  at  least  one  inch  across,  covered  by  a  yellowish 
slough  ;  the  peritoneum  covering  it  is  thickened  and  inflamed.  In 
upper  colon  there  is  considerable  necrosis,  involving  the  epithelium  in 


DIFKKRHNTIAL    DIACiNOSIS  259 

patches.  Ivungs  normal,  excepting  the  right  ventral  lobe,  which  is 
solid.  Bronchi  and  air  cells  of  this  lobe  completely  occluded  by  plugs  ; 
surface  bright  red,  mottled  with  yellowish  points — the  ultimate  air  cells 
filled  with  the  cellular  exudate.  Subpleural  ecchymoses  over  both 
lungs.  From  the  spleen  a  liquid  and  a  gelatin  culture  contained  only 
hog-cholera  bacteria.  They  were  very  numerous  in  cover-glass  prepar- 
ations from  this  organ. 

A  rabbit  inoculated  from  the  consolidated  lung  tissue  died  on  the 
seventh  day.  At  the  point  of  inociilation  a  pasty  mass  extends  to  abdo- 
men, only  subcutis  involved.  Spleen  engorged.  Single  acini  in  the 
liver  are  completely  necrosed,  yellowish  white.  In  both  organs,  hog 
cholera  bacteria.  Cultures  from  spleen  pure.  (Report  on  hog  cholera, 
1889). 

The  duration  of  the  disease  varies.  In  the  acute  septi- 
cemic type  it  ma}'  not  be  more  than  a  few  hours  or  a  day  at  the 
longest.  In  the  chronic  form  it  lasts  from  one  to  two  weeks, 
sometimes  longer. 

The  prognosis  is  noi  good.  Berry  states  that  recoveries 
are  not  rare.  Although  there  are  outbreaks  where  the  mortality 
reaches  from  Soto  loo  per  cent,  there  are  others  of  a  milder 
type  where  the  fatalities  do  not  exceed  50  per  cent. 

§  185.  Differential  diagnosis.  Hog  cholera  is  to  be 
differentiated  from  a  great  variety  of  dietary  disorders  and 
poisoning  from  alkalies  and  possibly  from  other  chemicals 
which  may  get  into  their  food.  *  Powdered  soap  has  been 
found  to  produce,  when  given  in  sufficient  quantities,  a  series 
of  symptoms  quite  similar  to  those  of  hog  cholera.  In  addi- 
tion to  the  many  as  yet  etiologically  undetermined  disorders 
often  producing  a  high  mortality  and  popularly  called  hog 
cholera,  infectious  pneumonia  or  swine  plague  and  tuberculosis 
are  to  be  distinguished. 

It  sometimes  happens  that  swine  when  kept  under  good 
hygienic  conditions  suffer  from  disorders  which  in  their  symp- 
toms resemble  hog  cholera,  but  anatomically  the  lesions  are 
varied  and  irregular.  A  few  such  enzootics  have  been  studied. 
A  few  have  been  described.  In  one  instance  B.  coli  communis 
seemed  to  stand  in  a  casual  relation  to  the  trouble.  Recently 
the  writer  has  studied  two   similar   enzootics   where   several 


26o  HOG    CHOLERA 

animals  died  and  where  the  lesions  were  very  few  and  exceed- 
ingly varied.  .In  some  of  them  there  were  healing,  intestinal 
ulcers.  The  bacillus  isolated  belonged  to  the  paracolon 
group.*  It  may  be  supposed  that  possibly  many  of  these 
mild  cases  (enzootics)  are  modified  hog  cholera.  At  present, 
however,  such  a  conclusion  does  not  seem  to  be  fully  justified. 

The  dietary  disorders  are  determined  b}-  their  history,  the 
irregularity  of  the  lesions,  and  the  failure  to  find  the  specific 
organism  of  hog  cholera  in  the  tissues  of  the  dead  animals. 
An  important  feature  is  the  fact  that  the  trouble  does  not 
extend  beyond  the  herd  or  herds  first  attacked  or  animals  fed 
and  kept  under  like  conditions.  The  amount  of  loss  from 
these  troubles  is  very  large.  They  are  very  often  confused 
with  and  mistaken  for  hog  cholera. 

Hog  cholera  must  also  be  differentiated  from  a  new  disease 
recently  described  by  de  Schweinitz,  which  resembles  acute 
hog  cholera  symptomatically,  but  which  is  caused  by  an 
unknown  organism  that  passes  through  a  Chamberland  filter. 

The  differentiation  of  hog  cholera  from  swine  plague 
depends  upon  the  specific  bacteria.  While  in  typical,  chronic 
cases  the  intestinal  lesions  in  hog  cholera  and  the  lung  affec- 
tions in  swine  plague  are  sufficient  to  distinguish  the  nature  of 
the  disease,  in  many  cases  the  variations  of  the  lesions  are  such 
that  diagnoses  must  depend  upon  the  bacteriological  findings. 
The  essential  differences  between  the  two  species  of  bacteria 
are  brought  out  in  the  comparison  appended. 

Bacillus  of  hog  cholera.  Bacterium  of  s-cvine  plague. 

1.  Rod-shaped  organism  with  i.  Elongated  oval  organism 
ends  rounded,  1.2  to  2.0//  in  0.8  to  1.5 /<  in  length,  0.6  to  o.8/< 
length,  0.5  to  08// in  width.  The  in  thickness.  The  size  varies  ac- 
size  varies  according  to  the  stage       ^°''^\"-?  ^o  the  stage  of  growth  and 

p             ,,         J    J-    •  •             J    .,.,  division  and  the  culture  media. 

ot   growth   and   division   and   the  ,  j       , 

,^               ,.  2.     From  old  cultures  it   usually 

culture  media.  .    .           ,.     ,         ,.,. 

_              ...  stains  entirelv.     when   m   process 

2.  From  cultures  it  stains  en-  ^^  division  as  found  in  the  organs 
tirely .  In  tissues  it  usually  stains  of  freshly  dead  rabbits  the  extrem- 
around  the  periphery  leaving  a  ities  stain  leaving  an  unstained 
light  centre.  central  band,  "polar  stain." 


*It  differed  from  the  hog-cholera  bacillus  in  not  saponifying  milk. 


DIFFERENTIAL    DIAGNOvSIS 


261 


3.  Actively  motile  in  liquids. 

4.  From  3  to  9  flagella  are 
demonstrable. 

5.  Vis<orous  growth  in  alkaline 
nutrient  liquids.  Less  vigorous  if 
liquids  are  acid  in  reaction. 

6.  Moderate  growth  on  potato. 
(Varies  according  to  reaction). 

7.  Distinct  growth  on   gelatin. 

8.  Saponifies  milk  in  from  3  to 
4  weeks. 

9.  Ferments  dextrose  with  the 
formation  of  acids  and  gas. 

10.  Does  not  ferment  lactose. 
Bouillon  containing  it  becomes 
strongly  alkaline.     No  gas. 

11.  Does  not  ferment  saccha- 
rose. Bouillon  containing  it  be- 
comes strongly  alkaline.     No  gas. 

12.  Destroyed  by  moist  heat  at 
58°  C.  in  15  minutes. 

13.  Dies  in  water  in  from  2  to  4 
months. 

14.  It  dies  in  the  soil  in  from  2 
to  3  months. 

15.  Rabbits  injected  subcutane- 
ously  with  o.i  cc.  of  a  bouillon 
culture  of  a  virulent  bacillus  will 
die  in  from  5  to  7  days.  Enlarged 
spleen,  necrotic  foci  in  liver. 

16.  Rabbits  inoculated  with  cul- 
ture of  an  attenuated  variety  live 
from  ID  to  20  days  or  recover.  The 
lesions  are  enlarged  spleen  and 
infiltration  of  the  follicles  in 
Peyer's  patches. 

17.  In  guinea  pigs  the  lesions 
are  practically  the  same  as  in  rab- 
bits. Death  occurs  in  from  7  to  12 
days. 


3.  Not  motile  in  li(|uids. 

4.  No  flagella  have  been  found. 

5.  (rrowth  moderate  or  feelile 
in  alkaline  nutrient  liquids.  No 
growth  if  liquids  are  acid. 

6.  No  growth  on  potato. 

7.  Feeble  or  no  growth  on 
gelatin. 

8.  Produces  no  apparent  change 
in  milk. 

9.  Ferments  dextrose  with  the 
formation  of  acids  but  no  gas. 

10.  Does  not  ferment  lactose. 
No  gas. 

XI.  Ferments  saccharose  with 
the  formation  of  acids. 

12.  Destroyed  by  moist  heat  at 
58°  C.  in  7  minutes. 

13.  Dies  in  water  in  from  10  to 
15  days. 

14.  It  dies  in  the  soil  in  from  4 
to  6  days. 

15.  Rabbits  injected  subcutane- 
ously  with  o.oi  cc.  of  a  bouillon 
culture  of  a  virulent  bacillus  will 
die  in  from  16  to  20  hours. 
Septicemia. 

16.  Rabbits  inoculated  with  a 
culture  of  an  attenuated  variety 
will  live  from  4  to  10  days.  The 
lesions  are  local  infiltration  of  pus 
cells  with  pleuritis,  pericarditis  or 
peritonitis. 

17.  Guinea  pigs  are  slightly 
less  susceptible  than  rabbits.  There 
is  more  local  reaction.  Death  oc- 
curs in  from  i  to  4  days. 


262  HOG    CHOLERA 

i8.     Pigs    are    not    usually    af-  iS.     Pigs  are  not  usually  affected 

fected  by  subcutaneous   injection  by  the  subcutaneous  injection  of 

of  small  quantities  of  culture.     If  small  quantities  of  culture.     The 

the  pigs  are  killed  within  i  to   3  bacilli  are  not  found  except  in  the 

weeks  the  bacilli  are  found  in  the  local  lesion.     In  a  few  cases  fatal 

local  lesion  and  certain  of  the  lyni-  results  are  reported, 
phatic  glands.       Fatal  results   are 
reported  in  a  few  cases  from  these 
injections. 

19.  Feeding    cultures    to    pigs  19-     Feeding    cultures    to    pigs 
which  have  fasted  for  24  hours  pro-  usually  produces  no  effect. 
duces   extensive  intestinal  lesions 

with  fatal  results. 

20.  Intravenous  inoculation  in-  20.  Intravenous  inoculation  in- 
to pigs  causes  either  an  acute  sep-  to  pigs  usually  produces  a  septic 
ticemia  or  a  chronic  form  of  the  form  of  the  disease  which  kills  in 
disease  in  which  are  produced  from  i  to  2  days.  Inoculation  into 
quite  typical  round,  firm,  elevated  the  lungs  causes  pleuritis,  usually 
ulcers.  accompanied  by  pneumonia. 

Dawson  pointed  out  the  .serum  reaction  as  a  possible 
means  of  diagnosis.  This  test,  however,  seems  of  little  value 
until  the  disea.se  has  run  a  course  of  many  days. 

v^  186.  Prevention.  As  hog  cholera  is  caused  by  a 
specific  organism,  the  first  fact  to  be  determined  is  to  find  the 
channel  or  means  by  which  it  can  be  carried  from  an  infected 
to  a  non- infected  herd.  The  thorough  investigations  which 
have  been  made  in  the  United  States  Bureau  of  Animal  Indus- 
try have  shed  much  light  upon  this  subject.  The  observations 
of  more  recent  years  have  confirmed  the  conclusion  reached  in 
the  earlier  reports  of  the  Bureau  concerning  the  means  of 
spreading  this  disease.  With  these  results,  the  pointing  out 
of  the  ways  by  which  the  virus  may  be  disseminated  and  the 
methods  necessary  for  checking  its  spread  is  no  longer  ques- 
tionable and  there  is  a  certainty  that  it  can  be  kept  away  from 
individual  herds  even  in  the  midst  of  widespread  epizootics. 
A  few  of  the  common  means  of  its  dissemination  are  worthy  of 
note. 

I.  The  virus  of  hog  cholera  is  frequently  introduced  into 
a  non-infected  locality  by  the  purchase  of  animals,  usually  for 


PREVENTION  263 

breeding  purposes,  from  herds  in  which  this  disease  exists  or 
has  existed  within  the  preceding  few  months.  These  animals 
are  usually  placed  among  the  home  raised  swine  without  quar- 
antine, thus  affording  every  possible  facility  for  starting  up  a 
new  outbreak.     The  reason  for  this  is  clear. 

2.  The  bacteria  can  be  carried  in  the  dirt  on  the  animals 
or,  as  is  most  usually  the  case,  the  pigs  may  have  been  but 
recently  infected  and  being  transferred  during  the  period  of 
incubation  they  develop  the  disease  later.  It  not  infrequently 
happens  that  the  purchased  animals  are  actually  suffering 
from  a  chronic  form  of  the  disease,  to  which  they  eventually 
succumb  but  meantime  infect  others.  In  purchasing  swine, 
therefore,  it  is  of  the  greatest  importance  that  the  history  ot 
the  herd  should  show  that  it  had  been  free  from  infectious 
disease  for  at  least  one  year.  In  addition  to  this,  newly 
purchased  swine  should  not  be  placed  immediately  after  ship- 
ment in  the  pens  with  the  home  stock,  but  they  should  be  kept 
in  a  separate  enclosure  until  all  danger  of  the  disease  has 
passed. 

3.  Swine  are  often  shipped  in  crates,  boxes  or  in  open 
cars  in  which  hogs  affected  with  hog  cholera  have  previously 
been  confined.  The  history  of  hog  cholera  contains  many 
illustrations  of  this  method  of  contracting  the  disease. 

4.  The  bacilli  of  hog  cholera  live  for  a  considerable  time 
in  water.  On  this  account  the  bacteria  from  outbreaks  which 
start  at  or  near  the  source  of  a  creek  or  small  river  may  be 
carried  in  the  current  and  infect  animals  which  wallow  in  the 
stream  many  miles  below.  By  keeping  swine  in  a  small  en- 
closure away  from  infected  streams  and  fields  the  disease  is 
often  prevented. 

5.  The  bacilli  of  hog  cholera  can  be  carried  in  the  dirt 
which  adheres  to  one's  shoes  or  to  farming  utensils.  It  not 
infrequently  happens  that  the  virus  of  this  disease  is  carried 
from  farm  to  farm  on  the  tools  taken  from  an  infected  place. 

6.  The  virus  may  be  carried  by  buzzards,  crows  and 
other  birds.      There  is  no  po.sitive  proof  that  the  virus  has  been 


264  HOG    CHOLERA 

disseminated  in  this  way  although  there  is  much  evidence  to 
support  such  a  theory,  particularly  in  the  South.  Several  out- 
breaks have  been  attributed  to  this  method  of  introducing  the 
virus.  The  hypothesis  emphasizes  the  necessit}'^  for  promptly 
disposing  of  the  dead  animals  instead  of  leaving  them  as  prey 
for  scavengers.  If  they  cannot  be  burned  it  is  best  to  cover 
the  bodies  with  a  liberal  amount  of  lime  and  bury  them. 

When  healthy  hogs  are  separated  from  those  suffering 
with  the  disease  it  is  a  safe  precaution  to  dip  them  in  a  disin- 
fectant to  kill  any  hog-cholera  bacteria  that  may  be  upon  the 
exterior  of  the  body. 

§  187.  Specific  treatment.  A  large  number  of  inves- 
tigations have  been  made  to  find  a  protective  vaccine  for  this 
disease  and  also  to  find  a  specific  serum  treatment.  Thus  far 
satisfactory  experimental  results  have  not  been  obtained.  In 
a  number  of  instances,  where  the  practical  application  of  the 
"serum  treatment"  has  been  made,  most  satisfactory  results 
followed,  but  the  reports  fail  to  give  evidence  of  an  accurate 
diagnosis  of  the  disease  treated.  In  these  cases,  the  better 
management  of  the  animals,  in  addition  to  the  serum,  would 
suffice  to  check  the  disease  if  the  trouble  was  of  a  dietary 
nature.  There  is  need  for  additional  investigation  along  these 
lines. 

REFERENCES. 

1.  Berry.  Swine  fever.  Jour.  Compar.  Path,  and  Thera.,\o\. 
XV  (1902),  p.  I. 

2.  Billings.  Bulletins  Neb.  Agric.  Expt.  Station,  iSSS.  Also 
many  special  publications  and  contributions  to  various  veterinary 
journals. 

3.  Dawson.  The  serum  diagnosis  of  hog  cholera.  Nezv  York 
Med.  Jour.,  Feb.  20,  1897. 

4.  DE  SCHWEiNiTz.  The  production  of  immunity  in  guinea  pigs 
from  hog  cholera  by  the  use  of  blood  serum  f  lom  immunized  animals. 
Annual  Report  of  the  Bureau  of  Animal  Industry,  U.  S.  Dept.  of 
Agric,  1898. 

5.  DE  ScHWEiNiTz  AND  DORSET.  A  form  of  hog  cholera  not 
caused  by  the  hog  cholera  bacillus.  Circular  No.  41,  U.  S.  Bureau  of 
Animal  Industry,  1903. 


TKTANUS  265 

6.  DoRSKT,  Bolton  and  McBrvdh.     The  etiologj-  of  hog  cholera. 
Bulletin  No.  j2.     Bureau  of  Animal  Industry^    U.    S.    Defii    Agric 
1905- 

7.  PETERS.  Serum  therapy  in  hog  cholera  Bulletin  No.  ^7, 
Uuir.  of  Neb.  Agric.  Exper.  Station,  1897. 

S.  Salmon  AND  vSmith.  Annual  Reports  of  the  Bureau  of  Ani- 
mal Industry,  1885-1895. 

9.  Salmon.  Special  report  on  hog  cholera,  its  history,  nature  and 
treatment.     U.  S.  Bureau  of  Animal  Industry,  iii8^. 

10.  Smith.  Zur  Kenntniss  des  Hog-cholera  Bacillus.  Central- 
hlattfiir  Bakter.  u.  Parasitenkunde,  Bd.  IX  ( 1891),  S.  253. 

11.  Smith.  Hog  cholera  group  of  bacteria.  Bulletin  No.  6,  U. 
S.  Bureau  of  Animal  Industry,  1894,  p.  9. 

12.  Smith  and  Moore.  Experiments  on  the  production  of 
immunity  in  rabbits  and  guinea  pigs  with  reference  to  hog  cholera  and 
swine-plague  bacteria.     Ibid.,  -p.  41. 

13.  Reed  and  Carroll.  Bacillus  icteroides  and  Bacillus  cholerae 
suis.     A  preliminary  note.      The  Medical  News,  Apr.  29,  1899. 

14-  Welch.  Report  of  investigations  concerning  the  causation  of 
hog  cholera,    fohns  Hopkins  Hospital  Bulletin,  Nov.  i,  1889. 

15-  Welch  and  Clements.  Remarks  on  hog  cholera  and  swine 
plague.  First  International  Veterinary  Congress  of  America  held  in 
Chicago.  III..  October,  1893. 


TETANUS 

Synonyms.      Lockjaw;  trisnuis. 

?^  188.  Characterization.  Tetanus  is  an  infectious  dis- 
ease (toxemia)  is  which  the  specific  organisms  are  locahzed  at 
the  place  of  inoculation.  It  is  characterized  by  spasmodic  con- 
traction of  the  muscles  referable  to  the  nervous  system  and 
by  the  absence  of  obvious  tissue  changes.  It  is  the  result  of  a 
specific  wound  infection.  All  mammalia  including  man  are 
susceptible.  It  occurs  most  frequently  in  horses,  asses  and 
mules  ;  next  to  them  in  the  smaller  ruminants  such  as  the 
sheep  and  goat  ;  it  appears  least  often  in  the  dog.  It  is  re- 
ported to  occur  rarely  in  birds  and  fowls  are  supposed  to  be 
immune.      The  human  species  is  very  susceptible. 


266 


§  iSg.  History.  Tetanus  is  one  of  the  diseases  that 
was  recognized  and  described  before  the  Christian  era.  It 
was  not  clearly  differentiated  until  the  discovery  of  its  specific 
cause  in  1884. 

§  igo.  Geographical  distribution.  Tetanus  is  reported 
to  be  more  prevalent  in  the  hot  climates  than  in  the  temperate 
ones,  while  in  the  very  cold  latitudes  it  is  rarely  if  ever  en- 
countered. It  is  more  frequently  met  with  in  some  districts 
than  in  others.  Although  very  common  in  certain  localities, 
it  is,  on  the  whole,  a  somewhat  rare  disease.  There  seem  to 
be  no  statistics  by  which  its  frequency  can  be  determined  in 
this  country,  but  in  certain  of  the  European  armies  this  has 
been  noted.  In  the  Prussian  army,  it  is  reported  to  occur 
once  in  a  thousand  cases  of  sickness  among  horses.  At 
Wiirtemberg,  Hering  reports  it  once  in  3000  ca.ses  of  disease 
among  the  horses  in  the  cavalry.  It  has  also  been  noted  that 
in  some  veterinary  hospitals  it  does  not  occur  for  long  periods, 
while  at  other  times  several  cases  may  appear  in  rapid  succes- 
sion.    It  is,  however,  a  wide  spread  disease. 

§  igi.  Etiology.  Te- 
tanus is  caused  by  a  slender 
bacillus  2  to  5  //  in  length. 
It  forms  spores  which  are 
at  the  end  of  the  organism 
giving  it  somewhat  the  ap- 
pearance of  a  pin.  On 
account  of  this  it  has  been 
designated  the  "pin  bacil- 
lus." It  is  anaerobic. 
This  organism  was  first  ob- 
served by  Nicolaier  in  1885, 
although  Carle  and  Rat- 
tone  showed  in  1884  that 
this  disease  could  be  transmitted  from  man  to  animals  by  inoc- 
ulation with  the  pus  from  the  local  lesion.  In  1889,  Kitasato 
isolated  the  bacillus   and    studied    it    in    pure   culture.     This 


Fig.  62.     Bacillus  teiani. 


ETIOLOGY  267 

bacillus  stains  readily  with  the  aniline  dyes,  especially  with 
carbolfiichsin.  It  takes  the  Gram  stain.  It  grows  well  in 
nutrient  gelatin,  agar  or  bouillon  and  on  blood  serum  at  the 
temperature  of  the  body  and  in  an  atmosphere  of  hydrogen  or 
in  the  absence  of  air  as  in  deep  agar  cultures.  The  addition  of 
a  little  grape  sugar  facilitates  its  growth.  It  has  the  distinc- 
tion of  producing  the  most  powerful  (poisonous)  toxin  of  any 
known  bacteria,  0.23  of  a  milligram  being  estimated  as  a  fatal 
dose  for  a  man  of  175  pounds  weight. 

The  fact  that  this  bacillus  is  an  anaerobe  renders  its  culti- 
vation of  little  practical  value  in  diagnosing  the  disease.  Al- 
though it  is  not  distributed  in  the  body,  it  can  usually  be 
found  in  cover-glass  preparations,  made  from  the  local  lesion 
and  stained  with  carbol  fuchsin. 

Bacillus  tctaiii  is  found  in  the  soil.  It  has  been  found  in 
hay  dust,  in  the  mortar  of  old  masonry,  in  the  dust  in  rooms, 
barracks  and  hospitals  and  in  the  arrow  poison  of  certain 
savages  in  the  New  Hebrides.  They  obtain  it  by  smearing 
their  arrow  heads  with  mud  from  crab  holes  in  the  swamps. 
It  is  reported  that  certain  savages  in  Africa  destroy  their 
enemies  by  putting  bits  of  broken  glass  mixed  with  certain 
soils  in  their  shoes.  The  cause  of  death  is  tetanus.  Mold 
rich  in  horse  manure  seems  to  be  the  most  favorable  abode  for 
it.  It  has  been  stated  that  it  exists  in  all  soils.  There  are 
good  reasons  for  believing  that  this  is  an  over-estimate  of  the 
wideness  of  its  distribution.  It  certainly  is  more  numerous  in 
some  localities  than  in  others. 

The  tetanus  bacillus  is  very  resistant,  especially  in  its 
spore  form,  to  destructive  agents  such  as  drying  and  the 
ordinary  disinfectants.  Kitasato  found  that  a  5  per  cent  solu- 
tion of  carbolic  acid  applied  for  ten  hours  failed  to  kill  the 
spores.  Tizzoni  and  Cattani  found  that  mineral  and  organic 
acids  produced  no  effect  upon  the  dried  spores,  von  Behring 
found  that  iodine  trichloride  possesses  a  strong  antiseptic  effect 
upon  them.  They  are  not  affected  by  the  gastric  fluids.  It 
has  been  noted  by  Kitt  that  the  dried  spores  in  pus  have 
retained  their  virulence  for  sixteen    months.     They    are    de- 


268  TETANUS 

stroyed  when  subjected  to  a  temperature  of  ioo°  C.  in  water  or 
steam  for  ten  minutes.  The  bacilli  in  the  vegetative  state  are 
readily  destroyed  by  the  usual  strong  disinfectants,  such  as  5 
per  cent  carbolic  acid. 

A  number  of  bacilli  closely  resembling  B.  tetani  have  been 
described.  This  renders  a  careful  study  of  the  suspected 
organism  necessary,  as  it  is  difficult  in  some  cases  to  determine 
B.  tetani  microscopically.  The  guinea  pig  inoculation  affords 
a  ready  means  of  differentiation  whenever  fresh  material  is 
available. 

§  192.  Mode  of  infection.  As  the  bacillus  of  tetanus 
is  widely  distributed  in  the  soil  and  consequently  on  articles 
contaminated  with  it,  the  most  common  modes  of  infection  are 
punctures,  scratches,  and  pricks  made  hy  splinters,  nails  or 
infected  instruments  (traumatic  tetanus).  It  may  follow 
slight  abrasions  of  the  skin  where  infected  earth  comes  in  con- 
tact with  the  lacerated  epidermis.  Infection  through  wounds 
in  the  intestinal  mucosa  do  not  seem  to  have  been  clearly  dem- 
onstrated. The  most  usual  method  seems  to  be  by  pricks 
and  nail  punctures,  in  which  case  the  virus  can  be  carried  well 
into  the  living  tissue  and  there  is  little  or  no  bleeding  to  wash 
it  out.  Infection  often  occurs  in  young  foals  and  lambs 
through  the  freshly  broken  umbilical  cord  (tetanus  neon- 
atorum). 

The  period  of  incubation.  The  shortest  period  which 
seems  to  be  reported  is  a  few  hours  and  the  longest  is  six 
weeks.  In  horses  the  period  of  incubation  is  usually  from  four 
to  twenty  days.  After  inoculation  with  pure  cultures  it  is 
from  four  to  five  days  and  in  sheep  from  two  to  four  days.  In 
guinea  pigs  inoculated  with  infected  soil  the  incubation  period 
is  usually  not  over  forty-eight  hours  and  often  less  than  that. 
Park  has  found  that  mice,  guinea  pigs,  rabbits,  rats, 
horses,  goats  and  a  few  other  animals  inoculated  with  pure 
culture  have  a  period  of  incubation  of  from  one  to  three  days. 
In  man  it  varies  from  one  to  twenty  days.  There  are,  how- 
ever, a  few  exceptionally  long  periods  reported.     It  has  been 


SY:\ii"r()Ms  269 

noted  by  Richter  and  others  that  the  shorter  period  of  iucuba- 
tion  the  more  severe  the  disease,  tlie  mortality  being  over  90 
per  cent  in  the  first  and  about  50  per  cent  when  the  symptoms 
were  slow  in  appearing. 

§  193.  Symptoms.  The  first  symptoms  are  often 
obscure  and  may  be  overlooked  for  several  daj's  or  they  may 
be  ushered  in  suddenly  with  violent  and  extensive  tonic 
spasms.  The  tetanic  spasms  usually  begin  in  the  muscles  of 
the  head  and  neck,  extending  from  these  to  the  muscles  of  the 
throat,  trunk  and  extremities.  It  often  happens  that  the 
spasms  first  appear  in  the  hind  quarters  and  extend  forward. 
There  is  stiffness  of  the  parts  affected.  If  in  the  head,  the 
muscles  of  mastication  are  first  attacked  with  spasms,  while  if 
the  hind  quarters  are  first  attacked,  there  are  usually  spasms 
of  the  muscles  of  the  tail.  The  muscles  at  the  site  of  inocula- 
tion are  frequently  the  first  to  show  spasms  and,  if  the  disease 
is  of  a  mild  type,  they  may  be  the  only  ones  to  exhibit  symp- 
toms. Friedberger  and  Frohner  have  grouped  the  muscles 
which  are  attacked  with  the  more  obvious  effects  upon  the 
appearance  of  the  animal.      They  are  as  follows  : 

1.  The  rmiscles  of  viastication.  The  contraction  of  these 
muscles  is  called  trismus  or  "lockjaw."  According  to  the 
degree  of  contraction,  the  jaws  remain  in  more  or  less  close 
contact,  rendering  prehension  or  mastication  difficult  or 
impossible. 

2.  The  other  muscles  of  the  head.  These  are  spasmodi- 
cally contracted  in  different  degrees.  Spasms  of  the  muscles 
of  the  ears  cause  the  ears  to  be  "pricked"  and  their  tips  to  be 
drawn  together  ;  of  the  recti  muscles  of  the  eyes,  cause  the 
eyes  to  be  retracted  in  the  orbit  with  protrusion  of  the  nictitat- 
ing membrane  ;  of  the  nose,  produce  dilatation  of  the  nostrils  ; 
of  the  dilator  of  the  upper  lip,  give  an  abnormal  shape  to  the 
opening  of  the  mouth.  The  muscles  of  the  tongue,  of  degluti- 
tion and  of  the  larynx  are  also  usually  attacked  by  spasms. 

3.  The  exteyisor  muscles  of  the  neck.  Contraction  of  these 
muscles  causes  a  stiff,  outstretched   carriage  of  the  head   and 


270 


TETANUS 


"ewe  neck."      The  muscles  of  the  neck  become  hard  and  tense 
to  the  touch. 

4.  The  extensor  muscles  of  the  back.  Spasms  of  these 
muscles  are  manifested  by  an  extremely  hard  condition  of  the 
muscles  of  the  back,  loins  and  croup.  Several  conditions  may 
arise  :  orthotonous  in  which  the  neck  is  stretched  out  and  the 
back  and  croup  are  carried  horizontally,  or  opisthotonous  in 
which  the  head  is  raised  or  drawn  back  and  the  vertebral 
column  slightly  depressed.  This  is  the  most  common  occur- 
rence. There  may  be  a  lateral  curvature  of  the  cervical  verte- 
brae which  is  uncommon  and  also  a  convex  curvature  of  the 
vertebrae  which  is  very  rarely  observed.  The  tail,  especially 
in  horses,  is  often  raised  and  occasionally  said  to  be  straight 
with  the  back. 

5.  The  jmiscles  of  the  limbs.  The  spasms  in  these  muscles 
make  the  limbs  stiff  and  cause  the  animal  to  assume  an  attitude 
in  which  the  fore  legs  are  extended  forward  and  laterally  and 
the  hind  ones  backward  and  laterally.  They  are  bent  at  the 
joints  only  with  difficulty.  The  contraction  of  the  muscles  of 
the  abdomen  gives  the  animal  a  tucked  up  appearance  and  the 
spasms  of  the  muscles  of  respiration  render  breathing  difficult. 

Besides  the  spasms  the  animal  shows  an  increased  reflex 
irritability  and  heightened  sensibility.  These  manifest  them- 
selves in  excitement,  timidity  and  intensified  muscular  con- 
tractions if  irritated.  Sweating  is  common,  especially  in  severe 
cases.  In  mild  cases  it  may  be  absent.  There  is  usually 
little  or  no  change  in  the  internal  temperature.  In  fatal  cases 
the  temperature  is  usually  constantly  high  toward  the  last. 
The  high  temperature  (104°  to  106°  F.)  usually  continues  for 
some  time  after  death.  Bayer  has  observed  in  a  horse.  24 
hours  before  death,  a  temperature  of  102°  F.  ;  one  and  a  half 
hours  before  death,  105°  F.  ;  at  the  moment  of  death,  111°  F.  ; 
and  fifty  minutes  after  death,  113°  F.  There  is  frequently  no 
increase  in  the  number  of  pulse  beats  until  severe  exacerba- 
tion sets  in.  The  frequency  of  the  pulse  is  much  greater  in 
animals  which  continue  recumbent  than  in  those  which  keep 
upon  their  feet.     The  pulse  is  often  hard  and    small    and    the 


MORHID    ANATOMY  27  I 

walls  of  the  arteries  are  spasmodically  tense.  In  many  cases, 
however,  it  is  full,  soft  and  easily  compressible.  There  is,  as 
a  rule,  an  increase  in  the  number  of  respirations,  which  may 
become  very  high  if  the  respiratory  muscles  are  attacked. 
The  number  varies  according  to  the  excited  condition  of  the 
animal.  The  respirations  may  increase  four  fold  without  a 
corresponding  increase  in  the  pulse  beat.  The  breathing  may 
reach  from  80  to  100  per  minute.  In  character  the  respirations 
are  shallow  on  account  of  the  fixed  condition  of  the  ribs  and 
the  spasms  of  the  muscles  which  compress  the  abdomen. 
There  may  be  cyanosis  and  catarrh  of  the  nasal  mucosa, 
coughing  and  in  fatal  cases  symptoms  of  hyperemia  and  edema 
of  the  lungs  and  often  pneumonia  (usually  aspiration  in 
nature).  There  is  constipation  due  to  lack  of  peristalsis  and 
the  rigid  condition  of  the  muscles  which  compress  the 
abdomen.  Micturition  becomes  less  frequent  and  more  difii- 
cult.  Complete  retention  of  urine  is  said  to  occur  in  some 
cases.  The  urine  has  a  high  specific  gravity  and  occasionally 
contains  albumen.  Some  animals  can  eat  readih'  while  others 
eat,  if  at  all,  with  great  difficulty.  They  like  to  play  with 
drink  set  before  them  and  often  try  to  satisfy  their  thirst, 
which  seems  to  increase  as  the  disease  advances.  In  fatal 
cases  the  animals  seem  to  be  perfectly  conscious  to  the  last. 
They  seem  to  be  possessed  of  a  feeling  of  terror. 

v^  194.  Morbid  anatomy.  The  gross  examination  of 
the  tissues  at  post-mortem  of  animals  dead  from  tetanus  is 
usually  negative.  It  has  been  pointed  out  by  Goldscheider 
and  Flatau  that  in  experimental  animals  there  are  certain 
characteristic  changes  in  the  motor  cells  of  the  anterior  horns 
of  the  spinal  cord  which  in  the  order  of  their  development 
depend  upon  the  concentration  of  the  toxin  or  virulence  of  the 
bacteria  injected  and  upon  the  duration  of  the  disease.  The 
changes  are  primarily  an  enlargement  of  the  nuclei,  which  at 
the  same  time  become  more  distinct  ;  then  follows  an  enlarge- 
ment and  disintegration  of  Nissl's  cell-granules  with  an 
enlargement  of  all  of  the  nerve  cells.     These  investigators  also 


2^2  rHTAJNUS 

found  that  where  antitoxin  had  been  used  it  had  a  distinct 
retarding  influence  upon  these  changes.  They  found  like 
lesions  in  the  spinal  cord  of  a  human  subject  dead  of  tetanus. 
Very  similar  results  have  been  obtained  by  Matthes,  Westphal, 
Goebel  and  others.  The  lesions  point  to  the  anterior  horns  of 
the  spinal  cord  as  the  primary  seat  or  origin  of  the  tetanic  con- 
tractions. The  changes  pointed  out  above  are  said  by 
Moschowitz  to  be  characteristic  of  tetanus  and  constantly 
found.  The  motor  ganglia  cells  of  the  anterior  horns  of  the 
spinal  cord  seem  at  present,  therefore,  to  be  the  most  likely 
source  of  the  spasms,  due  apparently  to  a  specific  affinity 
between  those  cells  and  the  tetanus  toxin.  It  is  possible  to 
explain  also  the  local  spasms  on  this  hypothesis  as  the  toxin 
elaborated  by  the  nerves  terminating  in  the  affected  region. 
The  experiments  of  Tizzoni  and  Cattani  suggest  the  possibility 
of  such  a  theory.  There  is,  however,  need  for  further  investi- 
gation on  this  subject. 

A  considerable  number  of  lesions  may  be  found  elsewhere 
in  the  body,  none  of  which  can  be  considered  as  characteristic 
of  the  disease,  but  which  are  secondary  to  the  tonic  contrac- 
tions. The  blood,  owing  to  lack  of  oxidation,  may  be  dark 
colored,  tarry,  of  a  greasy  appearance  and  tardy  in  coagula- 
ting. There  may  be  numerous  ecchymoses  and  sanious  exu- 
dates in  the  subserous  and  mucous  membranes.  The  lungs 
may  be  variously  affected  according  to  the  extent  of  the  trouble 
with  the  respiratory  muscles.  Thus  congestion,  edema, 
hemorrhages,  pneumonia,  emphysema  and  hypostatic  conges- 
tions have  been  described.  In  the  heart  there  are  usually  epi- 
and  endocardial  hemorrhages.  The  muscles  may  contain 
hemorrhages.  The  fibers  of  the  muscles  may  show  cloudy 
swelling,  a  loss  of  the  transverse  striae  and  changes 'in  the 
nuclei.  The  liver  may  be  swollen  and  abnormally  yellow  in 
color.  The  hepatic  cells  often  show  fatty  degeneration.  The 
spleen  is  often  swollen,  it  may  be  engorged  with  blood  or  soft 
and  flabby.  The  kidneys  may  or  may  not  show  degenerative 
changes.  The  bladder  is  usually  distended  with  urine  and  its 
mucous  membrane  is  often  sprinkled    with    ecchymoses.     The 


nil'l'KRKNTIAL    DIAGNOSIS 


273 


digestive  tract  may  show  areas  of  cougestion  and  ecchymoses. 

The  duration  of  the  disease  varies  in  different  species  and 
in  different  individuals  of  the  same  species.  In  the  horse  it 
may  last  for  two  or  three  days  only  or  it  may  continue  for 
several  weeks.  In  cattle  the  course  is  usually  less  rapid,  but 
it  rarely  runs  longer  than  two  weeks.  In  sheep  it  usually 
terminates  fatally  within  a  week  and  often  in  two  or  three 
days. 

i^  195.  Differential  diagnosis.  Tetanus,  while  possess- 
ing quite  characteristic  symptoms,  may  be  mistaken  for  a 
number  of  other  affections  or  specific  diseases.  Among  those 
which  should  receive  special  attention  are  cerebro-spinal  men- 
ingitis and  rabies  (for  the  symptoms  and  lesions  see  those  dis- 
eases), rheumatism,  eclampsia,  catalepsy,  convulsions  in  the 
newly  born  and  pyemic  polyarthritis  in  lambs  and  foals. 

The  symptoms  of  tetanus  which  are  perhaps  the  most 
diagnostic  are  (i)  the  continuous  tonic  spasms  of  different 
groups  of  muscles,  (2)  the  apparent  clearness  of  mind  (if  we 
may  attribute  such  a  quality  to  animals),  and  (3)  the  absence 
of  fever  in  the  beginning  of  the  symptoms.  The  general  atti- 
tude of  the  animal  is  also  of  much  value.  If  the  infected 
wound  can  be  found,  it  is  often  possible  to  obtain  cover-glass 
preparations  in  which  the  tetanus  bacilli  can  be  found.  Nega- 
tive results  are  in  this  case  not  to  be  considered  as  final,  for  it 
is  practically  impossible  to  make  these  examinations  suffi- 
ciently thorough  to  be  sure  of  the  absence  of  these  bacilli,  if 
they  are  not  found.  If  they  are  found  the  diagnosis  may  be 
considered  as  positive. 

In  poisoning  with  strychnine,  there  are  symptoms  which 
at  first  may  be  more  confusing.  This  form  of  poisoning 
usually  occurs  in  dogs  where  tetanus  is  rare,  and  again  in 
strychnine  poisoning  the  suddenness  of  the  attack,  the  rapidity 
of  the  course  and  the  increased  reflex  irritability  are  valuable 
diagnostic  features.  In  differentiating  tetanus  from  other 
affections  in  the  newly  born,  the  bacteriological  examination 
of  cover-glass  preparations  made  from  the  end  of  the  umbilicus 
may  be  of  much  a.ssistance. 


274  TETANUS 

§  196.  Prevention.  Owing  to  the  wide  distribution  of 
tetanus  bacilli,  precautions  can  consist  only  of  the  careful  and 
thorough  disinfection  of  all  wounds.  With  animals  at  pas- 
ture, it  is  impossible  often  to  know  of  the  wounds  until  it  is 
too  late  to  apply  this  measure.  In  stables  where  the  disease 
becomes  prevalent,  the  floors  and  siding  should  be  thoroughly 
disinfected  and  special  watchfulness  exercised  to  find  at  the 
earliest  moment  any  injury  by  which  infection  could  occur. 
The  practitioner  should  learn  as  soon  as  possible  the  tetanus 
infected  lands  and  stables  in  his  community  and,  knowing 
these,  give  wise  instruction  to  his  clients  to  take  such  precau- 
tions as  are  possible.  In  case  operations  are  to  be  performed 
on  animals  in  such  stables  an  immunizing  dose  of  tetanus 
antitoxin  may  be  administered.  This  practice  is  followed  in 
many  places  in  Europe.  If  the  present  knowledge  of  this 
disease  is  properly  availed  of,  there  should  be  only  occasional 
cases  which  as  yet  there  seems  to  be  no  way  to  avoid. 

§  197.  Tetanus  antitoxin.  It  was  first  pointed  out  by 
von  Behring  and  Kitasato  that  animals  could  be  made  immune 
to  tetanus  by  using  cultivations  of  the  tetanus  bacilli  which 
had  been  attenuated  with  iodine  trichloride.  The  blood  serum 
of  such  immunized  animals  has  the  power  to  immunize  healthy 
animals  against  the  disease  and  to  render  the  toxin  in  animals 
affected  with  tetanus  inert.  The  antitoxin  is  prepared  now, 
however,  by  injecting  horses  with  the  filtrate  of  bouillon 
cultures,  either  alone  or  with  a  quantity  of  antitoxin.  After 
the  first  dose  the  animal  becomes  tolerant  to  a  certain  degree 
so  that  by  repeated  and  constantly  increasing  doses  complete 
resistance  to  the  toxin  is  acquired.  When  this  point  is 
reached  the  serum  usually  possesses  a  strong  antitoxic  power. 
As  a  practical  remedy  for  the  disease  in  animals  the  recorded 
results  from  the  use  of  this  antitoxin  are  somewhat  contradic- 
tory. In  human  practice  the  results  are  similar.  Mosch- 
cowitz  has  collected  290  cases  in  man  where  it  has  been  used 
subcutaneously,  with  173  recoveries  and  117  deaths  or  a 
mortality  of  40.33  per  cent.     In  a  total  ot  48  cases  where  the 


REFERENCES  275 

antitoxin  was    injected    intracerebrally    23    recovered    and    25 
died,  a  mortality  of  52.08  per  cent. 

Some  interesting  experiments  suggested  by  Krokiewitz 
directed  toward  the  finding  of  a  specific  treatment  consist  in 
the  injection  of  an  emulsion  of  brain  substance.  Primarily 
this  method  of  treatment  is  based  upon  the  hypothesis,  set  up 
by  Goldscheider  and  Flatau,  who,  as  a  result  of  their  research 
came  to  the  conclusion  that  "The  morphological  changes  in 
the  nerve  cells  are  the  expression  of  a  chemical  process,  i.  e., 
of  the  chemical  combination  of  the  toxins  with  the  nerve 
cells.  Every  nerve  cell  possesses  atom  groups  which  have  a 
certain  aflSnity  for  the  atom  groups  of  the  tetanus  toxin  and 
are  able  to  combine  with  them."  Wassermann  and  Takaki 
substantiated  this  hypothesis  experimentally.  These  observers 
injected  into  experimentally  tetanized  animals  an  emulsion  of 
spinal  cord,  obtained  from  a  freshly  killed  animal,  to  test,  if 
possible,  whether  the  nerve  cells  of  the  dead  animal  also  have 
this  affinity  for  the  tetanus  toxin,  like  the  nerve  cells  of  the 
living  animal.  By  this  experiment,  they  have  come  to  the 
conclusion  that  every  part  of  the  nervous  system,  particularly 
the  brain  of  the  examined  animals  including  man,  has  a 
definite  and  positive  tetanus  antitoxic  power  ;  and  that  the 
injection  of  normal  brain  substance  into  experimentally 
tetanized  animals  has  the  power  to  save  life.  Further  work  in 
this  direction  is  necessary  to  fully  demonstrate  the  efficiency 
of  this  procedure. 

REFERENCES. 

1.  vonBehring  uxd  KitasaTO.  Ueber  das  Zustandekommeii 
der  Diphtherie-Immunitat  und  der  Tetanus-Immunitat  bei  Thieren. 
Deutsche  Med.  Wochenschrift,  Bd.  XVI  (1890),  S.  113. 

2.  KiTASATo.  Uber  den  Tetanusbacillus.  Zeit.  f.  Hygiene,  Bd. 
VII  (18S9),  S.  225. 

3.  KiTASATO.  Experimeutelle  Untersuchuugen  iiber  das  Tetanus- 
gift.     Zeit.  f.   Hygiene,  Bd.  X  (1891),  S.  267. 

4.  MoscHCowiTZ.  Tetanus,  a  study  of  the  nature,  excitant, 
lesions,  symptomatology,  and  treatment  of  the  disease,  with  a  critical 
summary  of  the  results  of  serum   therapy.     Studies  from    the  Depart- 


276  BLACK    LEG 

merit  of  Pathology  of  the  College  of  Physicians  and  Surgeons,  Columbia 
Umversity,  Vol.  Vll  (i8<)g-igoo}.  (M.  gives  pathology  and  antitoxin 
treatment,  summary  of  cases  and  full  bibliography. ) 

5.     McFari<and.     Tetanus  and  vaccination.      The  Jo urua I  of  Med- 
ical Research,  Vol.  VII  (1902),  p.  474.     (New  Series  Vol.  II). 


BLACK  LEG 


Synonyms.  Black  quarter;  symptomatic  anthrax;  quar- 
ter ill;  quarter  evil;  gangrenous  emphysema;  charbon  sympto- 
matiqjie;  Raiischbrauii. 

§  ig8.  Characterization.  Black  quarter  is  an  acute 
infectious  disease  of  cattle  characterized  by  the  development 
of  an  emphysematous  swelling  of  the  subcutaneous  tissues  and 
mu.scles.  These  lesions  are  usually  located  upon  and  ordinarily 
extend  over  the  greater  part  of  a  hind  quarter  or  of  a  shoulder. 
The  disease  does  not  spread  from  animal  to  animal  by  simple 
contact  but  the  infection  takes  place  apparently  from  a  com- 
mon source,  the  soil.  The  virus  seems  to  exist  in  the  soil  in 
certain  localities  only.  Like  tetanus,  it  is  a  disease  following 
a  wound  infection. 

Symptomatic  anthrax  is  a  disease  of  cattle,  sheep  and 
goats,  although  the  two  latter  species  are  rarely  attacked. 
Guinea  pigs  are  very  susceptible  to  inoculation.  It  is  reported 
that  horses,  asses  and  white  rats  develop  local  lesions  when 
inoculated  subcutaneously  with  the  virus.  Other  animals  seem 
to  be  immune.  In  cattle,  it  rarely  occurs  in  the  very  young, 
under  six  months,  and  in  adults  after  the  fourth  year. 

§  199.  History.  It  is  supposed  that  black  quarter  has 
existed  for  hundreds  of  years,  although  it  was  not  until  late  in 
the  last  century  that  it  was  positively  differentiated  and  recog- 
nized as  a  distinct  and  specific  'disease.  The  descriptions 
given  to  many  of  the  earlier  epizootics  designated  as  anthrax 
correspond  more  exactly  with  the  present  knowledge  of  black 
quarter  than  they  do  of  anthrax. 

In   1782,   Chabert  classified   the    various    anthracoid    dis- 


HISTORY  277 

eases  recognized  at  that  time  into  three  groups,  (  i)  anthrax 
fever,  where  the  disease  manifested  itself  without  external 
swelling,  (2)  true  anthrax,  where  the  lesions  consisted  at 
first  of  small,  hard  and  very  painful  swellings  followed  or 
accompanied  by  fever  and  other  general  symptoms,  and  (3) 
symptomatic  anthrax,  where  the  swelling  was  preceded  by  a 
rise  of  temperature,  loss  of  appetite  and  symptoms  of  general 
depression.  This  classification  was  held  for  nearly  a  century. 
BoutroUe,  in  1797,  refers  to  a  disease  which  he  called  mal  de 
adsse  (quarter  evil )  because  it  affected  the  animal  in  the  thigh. 
Viborg  described  the  disease  in  Denmark,  where  it  has  long 
been  known  to  the  laymen  and  designated  by  them  as  raslcsyge 
("rattle  disease"  ).  Its  clinical  features  were  very  accurately 
described  by  Walraff  in  1856.  In  1879,  Arloing,  Cornevin  and 
Thomas  proved  the  causal  relations  of  a  certain  microorganism 
to  this  disease  and  thus  established  its  specific  nature.  A 
year  later  (1880)  they  described  the  specific  microorganism 
and  demonstrated  that  the  disease  could  be  produced  by  inocu- 
lating susceptible  animals  with  it.  Since  that  time  both  the 
organism  and  the  disease  itself  have  been  studied  by  many 
investigators.  In  this  country,  it  has  been  under  investiga- 
tion during  the  last  few  years  by  the  Bureau  of  Animal 
Industry. 

§  200.  Geographical  distribution.  Black  quarter  ex- 
ists to  some  extent  in  nearly  every  country  in  the  world.  It 
is  reported  as  occuring  in  the  most  northern  latitudes  in  which 
cattle  are  kept,  as  well  as  in  the  temperate  and  tropical  zones. 
In  Europe,  it  occurs  on  the  pastures  on  the  Alps,  where 
for  five  months  in  the  year  the  ground  is  covered  with  snow 
and  ice  and  in  America  it  is  quite  common  in  certain  northern 
districts.  It  has  been  reported  from  Asia  and  from  Northern 
and  Southern  Africa. 

In  the  United  States,  it  prevails  to  a  greater  extent  than 
is  generally  supposed.  The  states  and  territories  which, 
according  to  the  reports  of  the  Bureau  of  Animal  Industry, 
suffer  most  from  it  are  Texas,  Oklahoma,  Kansas,  Nebraska, 
Colorado,  North  and  South  Dakota  and  Indian  Territory;  but 


278 


BLACK    LEG 


a  number  of  the  other  Western  States  are  badly  infected. 
Many  of  the  states  east  of  the  Mississippi  river  have  infected 
localities,  but  in  a  few  of  the  Eastern  and  Southern  states  it 
seems  not  to  exist.  During  the  last  few  years  infected  locali- 
ties have  been  found  in  New  York  where  there  has  been  an 
annual  loss  from  this  disease,  but  where  prior  to  recent  inves- 
tigations the  cause  of  death  has  been  attributed  to  poisoning. 

§  20I.  Etiology.  Black  leg  is  caused  by  Bacillus  chau- 
veaui.  This  organism  varies  from  3  to  6yw  in  length  and  from 
0.5  to  i./<  in  width.  The  ends  are  rounded  and  it  produces 
spores.  It  stains  readily  with  ordinary  aniline  dyes  and  also 
after  the  gram  method.  In  cultures  long  involution  forms  are 
often  observed.  It  is  anaerobic.  In  suitable  culture  media 
under  anaerobic  conditions  or   in   animal  tissues  (other  than 


\  \ 


\ 
^ 


^  1  \  " 

o       ' 


.\ 


Fig.  63.     Bacillus  of  black  leg  ivith  flagella  and  ivith  spores 
{after  Hutyra). 


blood)  it  multiplies  rapidly  with  the  evolution  of  gas.  The 
presence  of  spores  renders  it  very  resistant  to  natural  destruc- 
tive agencies  and  to  the  common  disinfectants.  The  bacillus 
of  black  leg  or  its  spores  are  supposed  to  gain  entrance  to  the 
tissues  of  animals  through  abrasions  of  the  skin  or,  possibly, 
the  raucous  membranes  of  the  mouth  or  intestine. 

The  period  of  incubation  is  not  known  in  cattle  but  it  is 
supposed  to  be  very  short.  Guinea  pigs  inoculated  with  a 
culture  of  the  organism  die  in  from  one  to  three  days. 


SYMPTOMS  279 

§  202.  Symptoms.  The  first  symptoms  may  be  either 
general  or  local  in  character.  Arloing,  Cornevin  and  Thomas 
believe  that  general  symptoms  always  precede  the  local  mani- 
festations. Norgaard  reports  finding  cattle  with  marked 
local  lesions  but  few^  animals  suffering  from  general  symp- 
toms, although  the  latter  may  have  preceded  the  former  and 
have  subsided. 

A  general  symptom  is  elevation  of  temperature,  reaching 
in  some^  cases  107°  F.  It  usually  falls  to  the  normal  or  even 
subnormal  before  death.  There  is  loss  of  appetite,  loss  of 
rumination  and  pronounced  depression.  Respiration  becomes 
accelerated,  reaching  140  per  minute  or  even  higher.  The 
animal  moves  with  difficulty  and  lies  down  frequently.  At 
first  the  visible  mucous  membranes  are  congested  and  within 
twelve  to  fifteen  hours  they  have  a  dirty  leaden  or  purplish 
color. 

The  local  symptoms  may  appear  on  different  parts  of  the 
body  except  below  the  knee  or  hock  joints  and  on  the  tail. 
They  are  less  frequently  found  about  the  head.  They  usually 
appear  on  the  thighs,  neck,  shoulders  and  lower  region  of  the 
chest.  The  swelling  is  at  first  small  and  painful.  It  spreads 
rapidly  and  may  in  a  few  hours  attain  to  a  large  size,  when  it 
becomes  characterized  by  a  crackling  and  a  gurgling  sound 
when  the  hand  is  passed  over  it.  On  percussion  it  gives  a 
clear,  tympanic  sound  due  to  the  collection  of  gas  in  the 
affected  tissues.  At  the  center  of  the  larger  swellings  the 
skin  becomes  dry  and  parchment-like,  cool  to  the  touch  and 
painless  upon  pressure.  If  lanced,  a  dark,  reddish,  frothy 
fluid  flows  from  the  wound.  It  emits  a  disagreeable  odor. 
In  some  cases  there  is  but  one  swelling  but  usually  there  are 
two  or  more  which  may  become  confluent.  The  lymph  glands 
adjacent  to  the  swellings  are  much  enlarged.  There  is  usually 
trembling  of  the  muscles,  which,  as  death  approaches,  may 
develop  into  violent  convulsions.     . 

Hun  has  pointed  out  the  interesting  fact  that  in  a  very 
large  percentage  of  cases  the  sweUings  appear  on  the  right 
side.     There  seems  to   be  no  explanation  given  for  this  local- 


28o  BLACK    LEG 

ization.      In  this  country,  records  are  wanting  of  observations 
on  this  point. 

Arloing  has  called  attention  to  a  mild  form  of  this  disease 
in  which  the  symptoms  are  slight  debility,  loss  of  appetite  and 
slight  local  swelling. 

§  203.  Morbid  anatomy.  After  death  the  carcasses  of 
animals  which  have  died  of  this  disease  soon  become  distended 
with  gas.  This  is  due  in  part  to  the  fermentation  in  the 
digestive  tract  and  in  part  to  the  formation  of  gas  in  the  sub- 
cutaneous tissues  due  to  the  presence  of  the  specific  bacillus. 
The  subcutaneous  distension  is  especially  marked  in  the  region 
of  the  swellings  but  it  extends  for  a  considerable  distance  from 
these  foci  in  the  direction  of  least  resistance.  The  tympanitic 
condition  often  causes  the  two  legs  on  the  upper  side  of  the 
carcass  to  extend  out  straight  without  touching  the  ground. 
A  dark,  blood-colored,  frothy  discharge  flows  from  the  nostrils 
and  anus.  Decomposition  takes  place  very  rapidly  except  in 
the  affected  muscles,  which  retain  a  sweetish-sour  odor  for  a 
considerable  time  after  other  parts  of  the  carcass  have  become 
putrid. 

The  skin  covering  the  swelling  is  often  affected  with  dry 
gangrene.  The  subcutaneous  connective  tissue  is  yellow, 
gelatinous,  infiltrated  with  blood  and  bubbles  of  gas  which 
escape  if  the  tumor  is  incised.  The  muscles  underneath  the 
tumors  are  of  a  dirty  brown  or  of  a  blackish  color.  At  other 
places  they  are  dark  red  or  dark  yellow  and,  when  exposed  for 
some  time  to  the  air,  they  may  have  a  golden  lustre.  They  are 
brittle,  putrid  and  very  rich  in  fluids.  They  crackle  on  palpa- 
tion. When  incisions  are  made  into  them,  blood  of  a  frothy, 
greasy,  tarry  appearance  and  of  a  sickish,  fetid  odor  issues 
from  them  when  they  are  squeezed.  The  fibres  of  the  muscles 
show  extremely  varied  degenerative  changes.  The  gases  that 
are  present  in  the  muscles  are  inflammable  and  burn  with  a 
bluish  flame  on  being  ignited.  They  are  said  to  have  but 
little  odor,  on  which  account  it  is  assumed  that  the}'  consist  of 
carburetted  hydrogen.     They  are  also  said  to  contain  carbonic 


MORBID    ANATOMY  28  I 

acid  but  no  oxygen.  An  exact  chemical  analysis  of  these 
gases  seems  not  to  have  been  made.  The  lymph  glands  near 
the  tumors  are  enlarged  and  full  of  blood.  They  contain 
hemorrhages  and  are  infiltrated  with  a  serous  fluid.  The 
afferent  lymph  vessels  are  sometimes  distended  with  gases, 
giving  them  the  appearance  of  strings  of  beads.  Changes 
similar  to  those  of  the  external  muscles  appear  in  the  muscles 
of  the  tongue  and  pharynx  when  the  disease,  as  may  happen 
in  rare  cases,  is  localized  on  the  oral  and  pharyngeal  mucous 
membranes. 

A  large  amount  of  blood-red  exudate  is  frequently  found 
in  the  abdominal  cavity.  In  other  cases  only  a  small  quantity 
of  a  serous  fluid  is  present.  In  still  others  no  changes  at  all 
appear.  The  abdominal  changes  seem  to  be  determined  by 
the  swelling  of  the  muscles,  that  is,  whether  it  has  or  has  not 
spread  to  the  peritoneum.  Yellow  gelatinous  and  hemorrhagic 
infiltrations  are  often  met  with  on  the  omentum,  mesentery 
and  in  the  neighborhood  of  the  kidneys.  The  mucous  mem- 
brane of  the  stomach  and  small  intestines  is  frequently  swollen, 
congested  and  infiltrated  with  hemorrhages,  in  which  case  the 
contents  of  the  intestine  are  bloody.  The  liver  is  hyperemic, 
but  the  spleen  is  usually  normal. 

In  the  thoracic  cavity,  the  pleurae  in  the  neighborhood  of 
the  swollen  parts  of  the  skin  and  mediastinum  are  sometimes 
hemorrhagic.  The  pleurae  may  ahso  show  large  ecchymoses, 
in  which  case  the  thoracic  cavity  contains  a  sero-sanious  exu- 
date. Hemorrhages  are  sometimes  present  in  the  lungs,  peri- 
cardium, myocardium  and  under  the  endocardium.  The 
muscular  tissue  of  the  heart  is  very  soft,  but  the  other  muscles 
show  only  slight  changes.  The  mucous  membrane  of  the 
bronchi  is  sometimes  hyperemic  and  sprinkled  with  hemor- 
rhages. 

The  blood  is  of  a  normal  color  and  coagulates  readily. 
The  fluids  of  the  muscles  have,  according  to  Feser,  an  acid 
reaction,  and  the  flesh  becomes  rapidly  putrid.  The  bacilli  of 
blackleg  are   found   only  in   small   numbers  if  at   all   in    the 


282  BLACK    LEG 

blood  during   life,    but   abundantly  a   few  hours  after  death. 
They  are  numerous  in  the  local  lesions. 

The  duration  of  the  disease  is  from  one  to  three  days. 
Occasionally  it  is  longer.     The  prognosis  is  grave. 

^  204.  Differential  diagnosis.  Black  quarter  is  to  be 
differentiated  from  anthrax,  the  "corn  stalk"  disease,  septi- 
cemia hemorrhagica  and  various  forms  ot  poisoning.  Usually 
the  localized  subcutaneous  lesions  are  sufficient  to  differentiate 
black  quarter  from  these  other  affections.  It  often  happens, 
however,  that  post-mortem  changes  have  so  modified  the  car- 
cass before  it  can  be  examined  that  the  diagnosis  is  question- 
able. In  this  and  all  doubtful  cases  or  where  only  small  por- 
tions of  tissue  are  sent  for  examination,  it  is  necessary  to 
resort  to  a  more  definite  method  or  methods,  such  as  the  mi- 
croscopic examination,  cultures  and  animal  inoculation. 

1.  Microscopic  examination.  Cover- glass  preparations 
made  from  the  fresh  tissues  will  ordinarily  exhibit  the  specific 
bacteria.  They  are  easily  distinguished  in  case  of  anthrax, 
black  quarter  and  often  with  septicemia  hemorrhagica,  while 
in  the  "cornstalk"  disease  and  cases  of  poisoning  character- 
istic bacteria  are  not  found.  It  is  important  to  eliminate  putre- 
factive bacteria,  when  the  animals  have  been  dead  for  some 
hours. 

2.  Cultures.  Ordinary  culture  media  inoculated  with 
the  tissues  from  a  case  of  anthrax  will  give  growths  of  the 
anthrax  bacterium,  and  from  cases  of  septicemia  hemorrha- 
gica that  of  Bad.  bovisepticum,  but  with  the  other  two  dis- 
eases they  will  remain  clear  if  uncontaminated.  The  black 
quarter  bacillus  will  grow  on  these  media  only  when  placed  in 
anaerobic  conditions.  In  case  of  the  "corn  stalk"  disease  the 
media  will  continue  to  be  clear. 

3.  Atiifjial  inociilatio7i.  In  guinea  pigs  inoculated  in  the 
deeper  subcutaneous  tissues  with  pure  cultures  of  black  leg 
bacteria  or  with  bits  of  tissue  from  the  affected  area  of  another 
animal  dead  from  the  disease,  death  ensues  in  from  one  to  two 
days.      It  is  preceded  by  a  raise  of  temperature,  loss  of  appetite 


I'REVENTION  283 

and  general  indisposition.  The  site  of  inoculation  is  swollen 
and  painful  and  drops  of  bloody  serum  maj^  sometimes  be  seen 
exuding  from  it.  At  autopsy  the  subcutaneous  cellular  tissues 
and  underlying  muscles  present  a  condition  of  emphysema  and 
extreme  edema.  The  edematous  fluid  is  often  blood  .stained 
and  the  muscles  are  of  a  blackish  or  blackish  brown  color. 
The  lymphatic  glands  are  markecily  hyperemic.  The  internal 
viscera  present  but  little  alteration  visible  to  the  naked  eye. 
In  the  blood  stained  serous  fluid  about  the  point  of  inoculation 
short  bacilli  are  present  in  large  numbers.  These  often  present 
slight  swellings  at  the  middle  or  near  the  end.  They  are  not 
.seen  as  threads  but  lie  singly  in  the  tissues.  If  the  autopsy  is 
made  immediately  after  death,  these  organisms  may  not  be 
detected  in  the  internal  organs,  but  if  not  made  until  after  a 
few  hours,  they  will  be  found  there  also.  In  early  autop.sies 
only  the  vegetative  forms  of  the  bacilli  may  be  found,  but  later 
(in  from  twenty  to  twenty-four  hours)  spore-bearing  rods  may 
be  detected.  With  the  "  corn  stalk  "  disease  the  inoculated 
animals  will  remain  well. 

§205.  Prevention.  In  checking  the  spread  of  the  dis- 
ease it  is  very  important  wherever  it  is  possible  to  remove  the 
well  animals  from  the  infected  field  and  to  restrict  the  sick  ones 
to  a  small  one.  The  swellings  should  not  be  opened  and  the 
discharge  scattered  over  the  field.  The  dead  animals  should 
be  burned  if  possible,  otherwise  buried  deeply  and  covered  well 
with  lime  as  soon  as  possible  after  death.  Birds  and  other 
animals  should  not  be  allowed  to  feed  upon  the  carcasses  and 
*  the  skin  should  not  be  removed.  Every  precaution  to  restrict 
the  spread  of  the  bacteria  of  this  disease  should  be  taken.  It 
is  very  desirable  to  thoroughly  disinfect  the  ground  where  the 
animal  lay  at  the  time  of  death.  The  spores  are  very  resistant 
both  to  disinfectants  and  the  natural  destructive  agencies  such 
as  sunlight  and  drying.  It  is  not  wise  to  use  land  upon  which 
animals  have  contracted  the  disease  for  grazing  purpo.ses  for 
susceptible  species. 

§  206.     Preventive   inoculation.       .Several    methods  of 


284  BLACK    LEG 

fortifying  exposed  animals  against  the  infection  of  sympto- 
matic anthrax  virus  have  been  proposed.  In  1880,  Arloing, 
Cornevin  and  Thomas  demonstrated  at  Chaumont  that  animals 
injected  with  the  filtrate  of  cultures  of  this  virus  into  the  jugu- 
lar vein  were  protected  against  inoculation  with  the  strong 
virus.  It  was  found,  however,  that  this  method  was  difiicult, 
as  the  vein  had  to  be  exposed  and  the  greatest  care  was  neces- 
sary to  prevent  infection  of  extra  vascular  tissue  in  introduc- 
ing and  withdrawing  the  syringe.  Later  these  investigators 
attenuated  the  virus  by  heating  it  to  a  temperature  of  100  to 
104°  C.  and  injecting  it  into  the  subcutis  of  the  shoulder.  This 
gave  a  partial  immunity  which  was  reinforced  after  eight  or 
ten  days  by  a  second  inoculation  of  a  virus  that  had  been 
heated  from  go  to  94°  C.  for  six  hours.  They  injected  the 
virus  where  the  subcutis  is  quite  dense,  such  as  at  the  end  of 
the  tail  where  onlv  local  swellings  would  occur.  This  process 
is  known  as  "  the  French  method,"  Arloing" s  or  the  "  Lyons 
method." 

In  1888,  Kitt  of  the  Veterinary  College  in  Munich,  after 
a  careful  investigation  of  the  subject,  proposed  a  single  injec- 
tion method  using  a  virus  attenuated  by  heating  at  a  tempera- 
ture of  from  85  to  90°  C.  for  six  hours.  A  single  injection  of 
this  vaccine  would  usuall}'  confer  immunity.  He  further 
modified  Arloing's  method  by  making  the  injections  in  the 
shoulder  regions  where  the  skin  is  looser  and  the  operation 
easier.  Later,  Kitt  made  further  important  investigations 
concerning  preventive  vaccines  for  this  disease. 

In  the  fall  of  1896,  investigations  looking  to  the 
preparation  of  a  black  quarter  vaccine  were  begun  in  the 
Bureau  of  Animal  Industr}'  at  Washington  by  Dr.  Norgaard 
under  the  direction  of  Dr.  Salmon.  The  various  European 
methods  were  tried.  The  one  finally  adopted  consists  of  a 
single  vaccine,  the  Arloing  principal  with  Kitt's  modification. 

The  material  used  for  the  vaccine  is  obtained  from  a  fresh 
blackleg  tumor,  by  pounding  the  muscle  tissue  in  a  mortar 
with  the  addition  of  a  little  water  and  squeezing  the  pulp 
through  linen  cloth.       The  juice  is  spread  in  layers  on   plates 


REFERKNCKS  285 

and  dried  quickly  at  a  temperature  of  about  35°  C.  This 
temperature  does  not  in  the  least  affect  the  bacteria,  and  the 
dry  virus  obtained  in  this  way  retains  a  high  degree  of  viru- 
lence for  two  years  or  longer. 

When  vaccine  is  to  be  prepared,  the  dried  material  is  pul- 
verized and  mixed  in  a  mortar  with  two  parts  water  until  it 
forms  a  semifluid  homogeneous  mass.  This  is  spread  in  a  thin 
layer  on  a  suitable  glass  dish  and  placed  in  an  oven,  the 
temperature  of  which  may  be  regulated  with  exactness.  The 
reason  for  mixing  the  dried  muscle  with  water  is  to  insure  a 
quicker  and  more  uniform  attenuation.  The  temperature  of 
the  oven  is  previously  brought  up  to  95°  to  99°  C,  and  the 
virus  is  allowed  to  remain  in  it  for  six  hours.  When  removed 
it  appears  as  a  brownish  scale,  which  is  easily  detached  from 
the  dish.  This  scale  is  pulverized  and  put  up  in  packages  con- 
taining lo  doses  each.  Before  it  is  used,  it  is  mixed  with 
10  c.  c.  water,  filtered  and  the  filtrate  injected  in  doses  of  one 
cubic  centimeter. 

REFERENCES. 

1.  Fisher.  Blackleg  in  Kansas,  and  protective  inoculation. 
Kan.  State  Agric.  Exper.  Station,   1901. 

2.  Lewis.  Symptomatic  anthrax.  Bulletin  No.  27.  Oklahoma 
State  Agric.  Exper.  Station,  1897. 

3.  Mayo.  Blackleg.  Bulletin  No.  6y.  k'an.  State  Agric. 
Exper.  Station,  1S97,  p.  108. 

4.  NoRGAARD.  Blackleg  in  the  United  States  and  the  distribution 
of  vaccine  by  the  Bureau  of  Animal  Industry.  Annual  Report  of  the 
Bureau  0/  Animal  Industry  U.  S.  Dept.  Agric.     1898. 

5.  NoRGAARD.  Blackleg.  Its  nature,  cause  and  prevention. 
Circular  No.  23.     U.  S.  Bureau  of  Animal  Industry,  1S9S. 

6.  Paouix.  Blackleg.  Bulletin  No.  12.  Mo.  Agric.  Exper. 
Station,  1890. 

7.  Peters.  Blackleg.  Its  nature,  cause  and  prevention.  Bulle- 
tin No.  65.     Neb.  State  Agric.  Exper.  Station,  1900. 

8.  SAI.MON.  Black  quarter.  Annual  Report  Bureau  of  Animal 
Industry,  U.  S.  Dept.  of  Agric.     1893-4. 


286  MALIGNANT    EDEMA 

MALIGNANT  EDEMA 

§  207.  Characterization.  Malignant  edema  is  an  acute, 
wound  infection  disease  of  domesticated  animals,  which  is  es- 
pecially characterized  b^'  edematous,  later  crepitating  tumors 
at  the  place  of  infection  due  to  Bacillus  oedematis  nialigiii. 

%  208.  History.  Crepitating  tumors  following  wounds, 
withdrawing  of  setons,  castration,  and  the  like  have  long  been 
known.  It  was  pointed  out  by  Girard  in  18 18,  that  creptita- 
ing  tumors  in  sheep  could  be  caused  by  subcutaneous  injection 
of  animal  tissue  taken  from  putrefying  tissue.  Chauveau 
(1873)  showed  by  experiments  performed  on  goats  that  the 
development  of  the  disease  stood  in  a  close  relation  to  living 
organisms  present  in  injected  putrescent  blood.  Pasteur,  in 
1887,  studied  more  closely  the  organism  and  named  it  Vibrio?i 
septiqtie.  He  obtained  it  in  pure  culture.  Later  Koch  and 
Gaffky  (1881)  studied  exhaustively  the  disease  caused  through 
contamination  by  contact  with  the  ground,  which  they  named 
malignant  edema.  Since  then  Kitt,  Jensen,  Sand  and  Leclainche 
have  studied  its  bacteriology,  while  Jensen  and  Sand,  v.  Ratz, 
Frohner,  Carl  and  others  have  made  valuable  contributions  to 
the  appearance  of  the  malady  among  domesticated  animals. 
Malignant  edema  is  a  wide  spread  but  not  a  common  disease. 

§  2og.  Etiology.  Maligant  edema  is  caused  by  5a<rz7/z^^ 
vedetnaiis  maligni  Koch  (  Vibrion  septiqiic  Pasteur).  It  is  de- 
scribed as  a  bacillus  resembling  that  of  anthrax,  but  somewhat 
more  slender,  rod-shaped,  and  spore  bearing.  The  ends  are 
rounded.  It  is  an  anaerobe.  In  artificial  cultures  as  well  as 
in  the  animal  body,  after  the  death  of  the  latter  the  bacilli 
grow  into  long  filaments.  Exceptionally,  living  animals  contain 
the  spore  bearing  bacilli  in  the  edematous  fluid  (Jensen  and 
Sand).  The  bacilli  stain  very  readily  with  aqueous  aniline 
dyes.  In  culture  media  containing  sugar  gases  are  formed, 
which  have  a  characteristic  disagreeable  odor.  The  inocula- 
tion of  a  pure  culture  into  the  deep  connective  tissue  of 
mammals  and  birds  produces  a  tumor  quickly   spreading  from 


MORHID    ANATOMY 


287 


the  place  of  inoculation  and  later  crackling  on   account   of  the 
formation  of  gas. 

Of  the  domestic  animals,  the  horse  is  the  most  susceptible 


Fig.  64.   Bacillus  oedematis  rnaligni  with  flagella  and  spores   ( Hutyra ) . 

to  natural  infection  ;  the  cow,  the  sheep  and  the  goat  are  less 
susceptible.     The  pig,  dog  and  cat  are  rarely  attacked. 

Infection  sometimes  follows  contusions  or  lacerations, 
sometimes  delivery,  when  in  the  latter  help  is  given  with  hands 
or  instruments  not  clean,  while  in  other  cases  it  occurs  such  as 
smallpox  vaccination,  castration,  shearing,  bleeding,  drawing 
setons,  subcutaneous  injections  where  unclean  syringes  are 
used. 

§  210.  Morbid  Anatomy.  On  the  expansion  of  a 
tumor  appearing  in  any  part  of  the  body,  the  connective  tissue 
is  distended  and  infiltrated  with  yellow  or  reddish  fluid  con- 
taining many  small  gas  bubbles,  which  emits  a  characteristic 
odor.  These  gelatinous  infiltrations  of  the  connective  tissue 
follow  between  the  deeper  layers  of  the  muscle.  The  muscle 
itself  is  often  sallow  or  dark  red  in  color  and  is  very  brittle. 
The  connective  tissue  in  places  seems  to  be  strewn  with  larger 
or  smaller  hemorrhages.  In  the  intestinal  cavity  there  is  a 
little  reddish,  serous  fluid  ;  the  peritoneum  is  deeply  injected. 
In  the  cases  in  which  malignant  edema  has  developed  in  con- 
nection with  parturition  the  uterus  is  insufficiently  contracted, 
the  subserous  connective  tissue  of  the  true  pelvis  and  the  walls 
of  the  uterus  are  edematously  infiltrated. 


288  MALIGNANT    EDEMA 

The  spleen  is  usually  not  affected.  Occasioually  acute 
tumors  with  gas  formation  are  found  in  the  pulp  (Frohner). 
The  liver  may  show  tumefaction.  The  mucous  membrane  of 
the  intestinal  canal  may  show  signs  of  acute  catarrh.  The 
lymph  glands  are  swollen.  The  lungs  are  hyperemic  and  for 
the  most  part  edematous.  The  muscular  system  of  the  heart 
shows  usually  a  high  degree  of  parenchymatous  degeneration. 
The  blood  clots  very  little.  The  body  quickly  becomes  putre- 
fied. The  fluid  pressed  out  of  the  crepitating  tumor  con- 
tains edema  bacilli  in  great  number,  associated  possibly  with 
other  bacteria. 

The  presence  of  the  bacilli  of  malignant  edema  in  the 
tissues  of  a  dead  animal  does  not  of  itself  prove  that  it  died  of 
this  disease.  These  bacilli  appear  very  often  in  the  intestinal 
contents  of  animals  which  feed  on  plants  in  company  with  other 
bacteria  and  on  that  account  are  able  after  the  death  of  the 
animal  to  multiply  in  its  tissues,  especially  when  the  blood  re- 
mains fluid  for  some  time,  as  for  example  after  a  sudden  death 
by  suffocation. 

^  211.  Differential  Diagnosis.  Malignant  edema,  if 
it  occurs  in  cattle,  can  be  easily  confused  with  symptomatic 
anthrax.  As  distinguishing  malignant  edema  are  the  occur- 
rence of  the  disease  in  a  region  where  symptomatic  anthrax  is 
not  native,  further  the  often  very  advanced  age  of  the  patient, 
the  occasional  localization  of  the  tumor  on  parts  of  the  body 
poor  in  muscle,  and  besides  the  insignificant  affection  of  the 
muscular  system  in  comparison  to  the  severe  affection  of  the 
connective  tissue. 

In  horses  and  sheep  the  development  of  a  crepitating  tu- 
mor with  a  fever  indicates  malignant  edema.  The  crepitation 
distinguishes  the  disease  from  anthrax  edema  as  well  as  from 
the  inflammatory  edemas  often  following  wounds  and  caused 
by  streptococci.  In  simple  subcutaneous  emphysema,  follow- 
ing skin  or  lung  wounds,  fever  rarely  occurs.  Finally  care 
must  be  taken  that  on  section  a  simple  emphysema  caused  by 
putrefaction  is  not  confused  with  a  crepitating  tumor  formed 
during  life. 


FOOT-ROT    IN    SHEEP  289 

^  212.  Prevention.  In  the  prophylaxis  of  the  disease 
the  wounds  of  the  skin  and  the  mucous  membrane  are  to  be 
kept  from  infection  with  the  soil,  those  which  are  already  in- 
fected are  to  be  disinfected,  while  after  difficult  delivery  in 
which  the  genital  passages  have  been  injured  a  thorough 
cleansing  of  the  latter  and  of  the  uterus  check  the  development 
of  the  trouble.  Test  animals  can  be  immunized  against  the 
virulent  infection  by  injection  of  tissue  juices  containing  spores 
after  heating  it  to  92°  C.  for  7  hours  (Leclainche  and  Vallee). 
These  inoculations  protect  only  against  malignant  edema  and 
not  at  the  same  time  against  symptomatic  anthrax,  as  Le- 
clainche and  Vallee  have  proved  in  contradiction  to  the  earlier 
experiences  of  Rouk  and  Duenschmann. 


FOOT-ROT  IN  SHEEP 

§213.  Characterization.  Foot- rot  in  sheep  is  an  infec- 
tiotis  disease  characterized  by  a  specific  inflammation  of  the 
tissues  just  above  the  horny  part  of  the  cleft  of  the  foot,  which 
extends  downward,  undermining  the  horny  portion.  It 
appears  in  epizootic  and  enzootic  forms.  Sheep  are  most  often 
attacked,  although  other  species  are  reported  to  be  susceptible. 

§  214.  History.  Foot-rot  has  been  recognized  for  more 
than  a  hundred  years.  It  has  been  described  from  various 
parts  of  Europe  by  Chabert,  Pictet  and  Gohier.  It  seems  to 
have  first  appeared  in  this  country  late  in  the  eighteenth  cen- 
tury. It  has  recently  been  investigated  by  Mohler  and  Wash- 
burn. They  found  a  specific  organism,  and  thus  differentiated 
it  from  the  streptococcic  infection. 

§  215.  Etiology.  The  cause  of  this  form  of  foot-rot  is, 
according  to  Mohler  and  Washburn,  an  anaerobic  organism, 
Bacillus  7iecropJioriis.  This  organism  is  isolated  with  difficulty 
from  these  lesions  because  of  the  association  with  it  of  other 
bacteria.  The  most  satisfactory  method  is  by  inoculating 
white  mice  or  rabbits  subcutaneouslv  with  the   diseased   tissue 


•290 


FOOT-ROT     IN     SHEEP 


from  their  organs 
time  required  to  kil 


\ 


\ 

V 


vV    \ 


\ 


V 


it  can  be  obtained  in   pure  culture.     The 
1  these   animals   is    usually    from    four    to 
twelve  days. 

The  period  of  incuba- 

\.  ,  tion  in  small  animals   is 

^\     N^         but  a  few  days.      In   the 
--^         1  naturally  contracted  dis- 

ease in  sheep  it  is  uncer- 
tain.    In  cases  produced 
by    inoculation    of    the 
I  \  J    -^  specific     bacillus     from 

\  "  ^  /  three  to  ten  or  more  days 

elapse  before  symptoms 
appear. 

§  216.  Symptoms. 
Lameness  is  the  first 
symptom  noted.  If  ex- 
amined prior  to  this, 
Mohler  reports  a  moist  area  of  the  skin  just  above  the  horny 
part  of  the  cleft  of  the  foot.  The  inflammatory  condition 
extends  rapidly  to  tissue  beneath  the  horny  part.  There  is 
often  a  discharge  of  a  thin,  purulent  fluid.  Mohler  states  that 
the  discharge  emits  a  pungent,  dis- 
agreeable odor  which  is  character- 
istic of  this  infection.  There  is 
emaciation  which  may  be  due  quite 
as  much  to  the  inability  of  the  lame 
^^f^'^  i^  '^^•^  sheep  to  procure  food  as  from   the 

^'^}Pf<fi<r'''^9.  %   Q-   c       specific  action  of  the  bacillus. 

The  duration  of  tlie  disease  varies 
from  a  few  weeks  to  several 
months.  The  cases  are  said  usual- 
ly not  to  terminate  fatally. 


Fig.  65.      Bacillus    iiecrophortis    {after 
Mohler) . 


b 

Fig.  66.     Necrotic  area 
the  liver  of  a    rabbit ; 


liver  cell,  B,  inflammatory 
zone.  A,  necrotic  center 
{Mohler). 


§  217,  Morbid  anatomy.  The 
tissue  changes  are  those  of  a  purulent  exudative  inflammation. 
As  the  process  undermines  the  horny   portion   of  the  hoof  it 


•MISCELLLANEOUS     INFECTIONS 


291 


may  slough,  and  granulating  tissue,  commonly  called  "fungoid 
growths,"  develop.  The  invasion  of  the  organism  and  the 
extending  of  the  necrosis  may  continue  until  the  tendons,  liga- 
ments and  even  the  bones  may  be  attacked.  There  is  going 
on  at  this  time  reparation  processes  which  usually  terminate  in 
a  peculiar  growth  composed  of  horny  elements,  dense  epithelial 
cells,  and  granulation  tissue  (Mohler), 

§  218.  Differential  diagnosis.  Foot-rot  in  sheep  is  to 
be  differentiated  from  inflammation  of  the  feet  caused  by  strep- 
tococcic infection,  purulent  inflammation  of  the  interdigital 
space,  the  stoppage  of  the  duct  of  the  interungulate  or  biflex 
gland,  and  contagious  foot-and-mouth  disease. 

REFERKNCES 

1.  Ernst.  Ueber  nekroses  und  den  nekrosebacillus  (streptothrix 
necrophora).     Monatsheft  f.  prakt.  Tier/ieilk.,  Bd.  XIV  (1902),  S.  193. 

2.  Mohler  and  Washburn.  Foot-rot  of  sheep,  its  nature, 
causes,  and  treatment.  Bulletin  No.  63.  U.  S.  Bureau  of  Animal 
Industry,  1904. 


MISCELLANKOUS  INFECTIONS  WITH  BACILLI 

§  219.  Enzootic  in  cattle  caused  by  a  bacillus  of  the 
enteritidis  group.  In  1902,  Mohler  and  Buckley=!^  described 
an  outbreak  caused  by  B.  enteritidis  among  cattle  in  a  stable  of 
21  animals  of  which  8  contracted  the  disease  and  died.  Three 
others  exhibited  the  early  symptoms. 

The  symptoms  were  first  refusal  of  food,  suspension  of 
urination  and  diminution  in  lactation.  There  was  excessive 
salivation  in  some  cases.  The  temperature  varied  from  102.7° 
to  104.1°  F.  The  visible  mucosae  were  congested.  There 
was  a  wild  expression  in  the  eyes  and  the   animals   were    very 


*MoHLER  AND  Buckley.  Report  on  an  enzootic  among  cattle 
caused  by  a  bacillus  of  the  enteritidis  group.  (Illustrated  and  bibli- 
ography).    Annual  Report  of  the  Bureau  of  Ant  ma  I  Industry,  1902. 


292  MISCELLANEOUS    INFECTIONS 

excitable.  The  gait  was  irregular.  Convulsions  set  in  prior 
to  death. 

The  duration  of  the  disease  varied  from  two  days  to  several 
weeks. 

The  morbid  anatomy  varied.  In  the  acute  cases  the 
anatomical  changes  were  very  slight.  The  most  noticeable 
and  characteristic  lesion  observed  consisted  of  petechial  hem- 
orrhages under  the  endocardium.  These  were  present  in  every 
case.  There  were  occasional  blood  extravasations  in  the 
intestinal  mucosa.  There  was  marked  injection  of  the  blood 
vessels  of  the  meninges  and  blood  tinted  fluid  in  the  cavity. 
The  chronic  cases  presented  a  wider  range  of  lesions  in  the 
organs. 

Cultures  of  the  bacillus  were  obtained  from  the  different 
organs.  The  bacilli  were  found  in  small  numbers  in  cover- 
glass  preparations  made  from  the  organs.  The  organism  was 
fatal  to  experimental  animals  and  to  calves.  It  was  more 
virulent  than  the  bacillus  of  hog  cholera  obtained  from  hogs 
dead  of  that  disease. 

Since  Gaertner  first  discovered  this  organism  in  1888  in 
the  meat  of  a  diseased  cow,  it  has  been  isolated  by  others  from 
both  animals  and  man.  It  has  been  found  to  produce  toxic 
properties  that  are  pathogenic  for  animals,  and  several  people 
have  been  reported  to  have  become  ill  from  eating  broth  made 
from  meat  containing  this  organism.  During  the  last  few 
years  several  bacilli  differing  slightly  from  Gaertner' s  bacillus 
have  been  isolated  from  cases  of  meat  poisoning. 

Bacilli  of  this  group,  or  at  least  of  closely  related  groups, 
have  frequently  been  found  to  stand  in  a  causal  relation  to  the 
lesions  with  which  they  were  associated.  The  more  import- 
ant of  these  are  Bacillus  typhi  mtirium  obtained  by  Loeffler  in 
1890  from  an  enzootic  among  mice,  the  bacillus  isolated  by 
Mereshkowsky  in  1895  from  the  ground  .squirrel,  and  Bacillus 
psittacosis  isolated  by  Nocard  in  1893  from  the  organs  of 
parrots. 

In  addition  to  these,  other  bacilli  have  been  found  appar- 
ently as  the  etiological  factor  in  isolated  cases  among  animals. 


GROUSE    DISKASE  293 

S  220.  Grouse  disease.  In  1887  Klein  described  a  dis- 
ease of  grouse  characterized  by  congestion  of  the  lungs,  liver 
and  kidneys  with  small  necrotic  areas  in  the  liver  and  areas  of 
redness  in  the  intestines.  The  di.sease  was  found  to  be  due  to 
a  bacillus  which  has  been  found  to  belong  to  the  colon  group. 
[The  author  has  studied  the  bacillus  of  the  Grouse  disease  a 
cultureof  which  was  obtained  from  Krahl  and  found  it  to  be 
B.  coli  cotnmiinis.']      Migula  designates  it  B.  scoticus. 

Quail  disease  (  Colibacillosis  tetraonidaruni) .  In  May  1 907 , 
Morse  {Circular  No.  109,  Bureau  of  Animal  hidustry)  described 
a  disease  of  quail  characterized  by  congestion  of  the  lungs, 
focal  necrosis  of  the  liver,  and  intestinal  ulceration.  He  found 
the  cause  to  be  a  member  of  the  colon  group  of  bacteria.  This 
seems  to  have  several  centers  of  infection  in  this  country. 
Several  species  of  quail  and  grouse  are  susceptible.  While 
there  are  strong  resemblances  between  this  affection  and  the 
grouse  disease  described  by  Klein,  Morse  assumes  that  they 
are  not  identical. 


CHAPTER    VII 

DISEASES    CAUSED   BY   BACTERIA 
FAMILY    SPIRILLACEiE. 


§  221.  General  Consideration  of  Spirillaceae.  This 
family  of  bacteria  has  thus  far  revealed  very  few  species  that 
are  pathogenic  for  domesticated  animals. 

§  222.     Diseases    of    fowls    caused    by    spirillaceae. 
The  disease  of  fowls  reported  to  be  caused  by  these  organisms 
has  not  been   found  in  this  country.     It  is  not  unlikely  that 
^     ^  some  one  or  more  of  the  many 

■'a»  *^        '  -         \  as  yet  mysterious  diseases  of 

\  poultry    may    be    caused    by 

members  of  this  family.  It  is 
interesting  to  note  that  spirilla 
are  not  uncommon  in  the  bac- 
terial contents  of  the  intes- 
tines. It  is  believed  that 
many  of  these  are  anaerobes, 
which  would  explain  the  diffi- 
culty encountered  in  trying  to 
isolate  them  in  pure  culture. 

Sakharoff  studied,  in  1891, 
a  peculiar  disease  of  geese  and 
showed  it  to  be  caused  by  a 
spirillum.  It  was  designated 
spirochacte  anserina.  Cantacuzene  has  studied  the  mode  of 
destruction  of  the  spirilla.  He  found  that  they  are  destroyed 
by  and  within  the  macrophages  of  the  spleen. 

The  morbid  anatomy  in  the  affections  caused  by  the 
spirilla  appear  to  be  largely  engorgement   of  the   spleen    and 


Fig.  67.   Spirochaete  anserina  fro'Di 

the  blood  of  a  goose  {after 

Cantacuzene) . 


Sl'IRILLOSIS  OF  CATTLE  295 

swelling  of  the  liver  with  fatty  degeneration  of  the  parenchy- 
matous tissue.  The  heart  muscle  is  sometimes  affected. 
Areas  of  necrosis  have  been  described  in  the  solid  viscera. 

It  is  stated  that  the  blood  of  the  diseased  fowl  is  not 
infectious  48  hours  after  it  has  been  removed  from  the  fowl 
but  that  if  injected  into  a  healthy  fowl  it  will  confer  immunity 
against  a  virulent  infection.  Marchoux  and  Salimbeni  found 
that  if  the  fresh  blood  of  the  diseased  fowl  was  heated  for  5 
minutes  at  a  temperature  of  55°  C.  it  would  confer  immunity 
but  if  it  was  heated  for  10  minutes  this  property  was  lost. 

§  223.  Spirillosis  of  cattle.  Theiler  found  spirilla  in 
a  few  cattle  in  South  Africa.  The  animals  were  suffering  with 
"  red  water  "  with  possibly  one  exception.  He  sent  prepara- 
tions of  these  to  Laveran  who  designated  them  Spirilhim 
Theileri.  Theiler  made  a  number  of  inoculations  with  the 
blood  of  animals  infected  with  the  spirilla  with  negative 
results.  The  following  description  of  the  spirillum  is  quoted 
from  Theiler' s  report  : 

"  The  microorganism  in  question  is  a  typical  spirillum, 
and  varies  considerably  in  its  length.  The  longest  microbes 
measure  from  20  to  30//.  They  are  somewhat  thinner  at  both 
ends,  otherwise  the  thickness  is  about  the  same  throughout 
the  whole  length — viz.,  about  .25  to  .\o  }.i.  The  corkscrew-like 
forms  are,  as  a  rule,  predominant,  but  there  are  other  forms 
which  are  atypical  in  appearance  and  also  shorter.  For 
instance,  the  parasite  may  show  itself  as  a  simple  curved  line 
without  any  spiral  curves,  representing  sometimes  the  shape 
of  S  ;  it  may  also  be  completely  doubled  up,  both  ends  may 
meet  and  take  the  shape  of  a  ring,  or  both  ends  may  cross  each 
other  and  also  form  a  loop.  These  loops  may  be  of  different 
shapes  and  sizes.  Double  loops  may  also  be  found.  It  is 
somewhat  difficult  to  describe  all  the  various  forms,  but  they 
can  be  easily  imagined,  considering  that  the  spirillum  is  a  very 
flexible  and  agile  parasite. 

"  In  preparations  made  by  placing  a  cover-glass  on  a  drop 
of  fresh  blood  the  microorganisms  are  easily   detected.     Some 


296 


DISEASES    CAUSED     BY    SPIRILLACEAE 


of  the  red  corpuscles  show  a  slight  irregular  motion,  and  when 
closely  watched  it  may  be  noticed  that  this  disturbance  may 
proceed  in  a  certain  direction,  or  again  whirl  round  in  the 
same  place.  When  examined  under  a  high  power  (i-i2th 
inch  obj.)  the  agile  spirillum  is  usually  seen  attached  to  one  or 
more  red  corpuscles.  Sometimes  it  is  curled  all  round  a  red 
or  white  corpuscle.  As  soon  as  the  organism  becomes  free 
and  begins  to  travel  through  a  clear  space,  a  characteristic 
undulating  movement  is  visible,  which  continues  until  it  finally 
attaches  itself  to  some  other  blood  corpuscle.  This  motion 
may  be  noticed  for  some  time  ;  it  then  becomes  relaxed,  and 
finally  slackens  down  completely.  I  have  observed  the 
movements  in  preparations  which  were  twentj'-four  hours  old. 
"Staining  of  the  organism  may  be  obtained  with  any  of 
the  aniline  dyes  used  in  bacteriology,  viz.,  methylene-blue, 
fuchsin,  thionin.  Good  preparations  were  obtained  with 
Ivaveran's  modification  of  Romanowsky's  stain,  and  also  with 
Azur  II.  In  using  the  last  two  mentioned  methods  no  chro- 
matic bod}'  could  be  traced,  such  as  is  present  in  parasites 
belonging  to  the  protozoa. 

"Cultivations  on  the 
usual  artificial  mecia  were 
repeatedly  tried,  but  al- 
ways with  negative  results. 
The  same  has  been  found 
to  be  the  case  with  all  the 
above-mentioned  different 
spirilla  found  in  men  and 
birds.  " 


u^ar^J^^ 


?^  224.  A  disease  of 
the  pig  due  to  spiro- 
chaetes.  Dodd  has  recently 
described  a  spirochaete 
which  he  found  in  a  pig 
sent  to  the  government 
laboratory  in  Pretoria.  The 
examination  showed  very  few  morbid  changes   in    the    tissues 


Spirochaetes  from  the  lesions 
in  the  skin  of  a  pig  {after  Dodd). 


OTIIKR    SPIKOCHARTES     FOUND    IN    ANIMALS 


297 


but  the  skin  was  sprinkled  with  dark  hemorrhagic-like  spots. 
From  scrapings  of  these  lesions  he  was  able  to  find  the  organ- 
ism. It  is  described  as  long  and  very  slender,  its  length  vary- 
ing from  9  to  26  //.  Both  extremities  are  pointed.  The  spiral 
forms  predominate  but  in  the  same  preparation  curved  or 
simply  long  straight  threads  were  observed.  They  appeared 
singly,  in  pairs  and  in  clumps.  It  was  difficult  to  distinguish 
It  in  the  unstained  preparation.  It  stains  well  with  any  of  the 
ordinary  aniline  dyes  but  does  not  retain  the  coloring  matter 
after  being  treated  by  the  Gram  method. 

S  225.  Other  spirochaetes  found  in  animals.  Bon- 
hoff  (1905)  described  a  .spirochaete  found  in  the  pustules  of 
vaccinia  of  the  calf.  Martoglio  and  Carpano  found  a  .spi- 
rochaete in  the  blood  of  the  Abyssinian  sheep.  It  exhibited 
from  three  to  ten  regular  spirals  and  measured  from  10  to  20// 
in  length  and  from  2  to  4  //  in  breadth.  The  extremities  were 
tapered  and  it  did  not  stain  by  Gram's  method.  It  could  not 
be  cultivated  on  any  media  used.  Neither  flagella,  spores  nor 
chromatin  were  discovered.  Two  spirochaetes  were  often 
seen  attached  throughout  their  length  and  apparently  fused 
together  at  one  extremity  as  through  they  had  been  produced 
by  longitudinal  fission.  This  parasite  was  present  in  the  blood 
plasma.  As  in  the  case  with  the  Sp.  Theileri  the  disease  could 
not  be  reproduced  in  any  of  the  animals  inoculated  with  the 
infected  blood  or  even  in  sheep.  This  organism  was  de- 
scribed by  Blanchard  as  Sp.  ovma. 

According  to  Bizzozero  the  stomach  of  the  dog  always  con- 
tains numbers  of  extremely  slender  spirochaetes  formed  of  from 
three  to  seven  turns  and  from  3  to  8  //  in  length  lodged  in  the 
interior  of  the  gastric  cells.  These  were  found  in  the  Norway 
rat,  cat  and  dog.  In  the  latter  they  have  been  found  to  be 
constantly  present. 

The  principal  species  of  the  spirochaeta  that  have  been 
described  are  the  Sp.  plicatilis  Ehrenberg,  in  1838.  It  is 
common  in  stagnant  water  and  often  attains  a  length  of  100  to 
200  i.1.  In  1875,  Cohn  described  Sp.  buccalis  which  is  tapered 
at  both  extremities  and  common  in  the  dental  tartar  and  in  the 


298  DISEASES    CAUSED    BY     SPIRILLACEAE 

saliva.  In  the  same  year  the  Sp.  Obertmieri  was  named  by 
Cohn  after  its  discoverer  as  the  cause  of  recurrent  fever  in 
man.  This  organism  varies  from  15  to  30  //  in  length,  is  very 
thin  and  tapered  at  both  extremities.  In  1905  Schaudicn  and 
Hoffmann  described  a  spirochaete  which  is  believed  to  be  the 
cause  of  syphilis.      It  is  known  as  Treponema  pallidum. 

REFERENCES 

1.  Cantacuzene.  Recherches  sur  la  spirillose  des  oies.  Ann. 
de.  V  Inst.  Pasteur,  Vol.  XIII  (1S99),  p   529. 

2.  DoDD.  A  disease  of  the  pig,  due  to  spirochaeta.  Jotir.  Coinpar. 
Path,  and  Thera  ,  Vol.  XIX  (1906),  p.  216. 

3.  Gabritschewskv.  Beitrage  zur  Pathologic  und  Serotherapie 
der  Spirochaten-Infektionen.  Centratd.J.  Bakter.,  Bd.  XXIII(  189S),  S. 
365,  und  778. 

4.  Levadite  et  Maxoxeliax.  Xouvelles  recherches  sur  la  spi- 
rillose des  poules.     Ann.  de  /'  Inst.  Pasteur,  Vol.  XX  (1906),  p,  592. 

5.  Sakharoff.  Spirochaeta  anserina  et  la  septicemie  des  oies. 
Ann.  deV  Inst.  Pasteur,  Vol.  V  (1891),  p.  564. 

6.  Theiler.  Spirillosis  of  cattle.  Jour.  Coinpar.  Path,  and 
Thera..  Vol.  XVII  (1904),  p.  48. 


CHAPTER    VIII 


DISEASES    CAUSED   BY   FUNGI. 


ACTINOMYCOSIS. 

Syniptoins.     Lumpy  jaw  ;  wooden  tongue;  big  head. 

^  226.  Characterization.  Actinom3COsis  belongs  to 
the  class  of  affections  known  as  the  infectious  granulomata.  It 
is  a  chronic  disease  determined  by  the  presence  of  a  specific 
cause — the  ray  fungus — which  by  irritation  stimulates  the  for- 
mation of  new  growths  consisting  of  round  cells,  epithelioid 
cells,  giant  cells  and  fibrous  tissue.  The  neoplasms  appear  as 
tumors  having  either  a  tendency  to  develop  into  large  and 
hard  masses  or  to  suppurate.  It  has  been  suggested  that  the 
suppuration  was  due  to  a  secondary  infection  by  pyogenic 
bacteria. 

Cattle  (genus  Bos)  are  most  often  attacked.  Horses, 
dogs,  pigs,  sheep  and  elephants  are  slightly  susceptible  and  a 
few  cases  have  been  reported  in  each.  Men  are  susceptible 
but  this  disease  is  rarely  found  in  the  human  subject.  Other 
species  seem  to  be  immune. 

§  227.  History.  The  early  history  of  this  disease  is 
quite  obscure.  Prior  to  the  discovery  of  its  specific  cau.se,  it 
was  much  confu.sed  with  other  diseases  resembling  it  more  or 
less  closely  in  certain  gross  appearances.  It  was  designated 
by  a  variety  of  names,  the  more  common  of  which  are  swelled 
head,  lumpy  jaw,  big  head,  fibroma,  sarcoma  and  osteosar- 
coma. It  is  popularly  known  in  the  United  States  as  "  lumpy 
jaw"  and  in  Europe  as  "wooden  tongue."  The  popular 
names  were  probably  suggested  by  the  character  of  the  lesions, 
which  differ  to  a  marked  degree.  It  was  recognized  as  a 
specific  disease  by  Rivolta  in  1868,  by  Perroncito  in   1875  and 


300 


ACTINOMYCOSIS 


by  Bollinger  in  1877.  The  ray  fungus  was  undoubtedly  ob- 
served prior  to  this  by  Lebert  and  Robin,  both  of  whom  failed 
to  recognize  it  as  a  vegetable  parasite. 

The  fungus  was  carefully  described  by  Dr.  Harz,  a  botan- 
ist, who  gave  it  the  name  actinomyces  or  ray  fungus.  Bolin- 
ger  was  the  first  to  carefully  study  the  disease  in  cattle  and  to 
demonstrate  the  power  of  the  ray  fungus  to  produce  disease. 
With  this  discovery  of  Bollinger  in  1877,  actinomycosis  be- 
came recognized  as  a  definite,  specific  disease  which  could  in 
most  cases  at  least  be  differentiated  from  the  other  affections 
with  which  it  had  hitherto  been  confused.  In  1845  von  Lang- 
enbeck  of  Kiel  observed  and  made  drawings  of  peculiar  bodies 
in  a  case  of  vertebral  caries  in  man  which  it  is  now  believed 
were  rosettes  of  the  ray  fungus.  In  1878,  Israel  demonstrated 
the  disease  in  man.  Since  that  time  it  has  been  carefully 
studied  and  described  by  a  number  of  investigators. 

s5  228.  Geographical  distribution.  Actinomycosis  is 
quite  widely  distributed  throughout  North  and  South  America 
and  Europe.  It  is  much  more  prevalent  in  certain  countries 
and  districts  than  in  others.  The  observation  has  been  made 
that  animals  pastured  upon  low  lands  and  in  river  valleys  are 
more  liable  to  contract  it  than  those  feeding  upon  high  and 
dry  ground.  It  has  also  been  noted  that  cattle  fed  upon  rough 
or  coarse  forage  are  more  prone  to  the  disease  on  account  of 
abrasions  of  the  buccal  mucosa  than  those  kept  upon  less 
harsh  food. 

It  is  very  difficult  to  procure  reliable  statistics  concerning 
the  extent  to  which  it  occurs.  The  observations  which  have 
been  made  at  the  union  stock  yards,  Chicago,  show  one  case 
of  actinomycosis  in  from  1600  to  1700  cattle.  The  statistics 
from  the  abattoirs  in  Berlin  show  one  case  to  4150  cattle  and 
one  in  8000  pigs.  These  figures  do  not,  however,  indicate  the 
extent  of  the  disease  among  the  farm  animals,  as  they  are 
collected  from  those  animals  presented  for  slaughter  only.  At 
the  clinic  of  the  New  York  State  Veterinary  College  there  is 
presented  for  treatment  a  very  few  cases    each    year.      In    the 


ETIOLOGY  301 

Mississippi  X'alley  and  in  the  South-west  it  seems   to  he    more 
prevalent  than  it  is  east  of  the  Allej^hany  Mountains. 

§  229.  Etiology.  Actinomycosis  is  produced  by  a 
fungus,  Cladothrix  acthio»iyccs,  commonly  known  as  the  "ray 
fungus."  ='^  The  disease  is  the  result  of  its  multiplying  in  the 
tissues  and  not  from  the  elaboration  of  a   toxin.     Undoubtedly 


Fig.  69.     A  rosette  of  the  ray  fungus  together  ivitlt  different  forms  of 
tlic  single  club  ends.     X  ^500.  {After  Crookshank) . 

the  bacteria  often  associated  with  the  fungus  in  suppurating 
lesions  are  of  some  significance.  Wright  states  that  he  believes 
they  play  an  important  part  in  the  extension  of  the  disease. 
The  fungus  appears  as  minute,  yellowish  granules  in  the 
lesions.      When  examined  microscopically,  these  granules  are 

*The  cladothrix  is  placed  among  the  higher  bacteria.  There  are 
many  varieties  of  the  actinomyces.  Until  they  are  better  understood  it 
seems  better  to  group  them  with  the  fungi. 


Fig.    70.       Photograph    of  a  young   actinoniycotic  groivth  under  low 
power,  showing  clumps  of  the  ray  fungus. 


ic    \  • 


.^  .•'••"   •» 


Fig.  71.     Photograph  under  higher  magnification  of  one  of  the  clumps 
of  the  ray  fungus  shoiving  giant  cells  about  the  clump  of  fungi. 


ETIOLOGY 


303 


found  to  be  made  up  of  rosettes  varying  in  size  from  10  to 
200//  in  diameter,  the  average  size  ranging  from  301040/^. 
This  fungus  can  be  cultivated  on  artificial  media.  It  stains 
somewhat  feebly  with  the  aniline  dyes. 

The  rosettes  are  composed  of  a  number  of  club-shaped 
structures  (rays),  radiating  from  the  central  mass  which  is 
composed  of  the  mycelial  part  of  the  fungus.  The  club-shaped 
bodies  vary  in  size  but  usually  they  are  from  i  to  10 /<  long. 
The  rays  are  connected  with  the  central  portion  by  fine  thread- 
like structures  which  are  not  readily  demonstrated.  In  tear- 
ing or  crushing  the  rosette,  the  clubs  break  off  at  or  near  their 
junction  with  the  mycelial  threads.  Some  investigators  have 
mentioned  a  polymorphous  form  of  actinomyces  in  which 
coccoid  and  rod-shaped  structures  are  found.  These  are  doubt- 
less the  ends  of  the  clubs  which  first  appear  in  focusing  on  a 
rosette. 

The  mycelial  threads  are  wider  in  some  portions  than  in 
others.  In  the  narrowest  places  the  walls  seem  to  touch  each 
other.  Whether  this  irregularity  is  natural  or  the  result  of 
twisting  the  mycelial  thread  is  not  determined.  The  myce- 
lium is  much  more  difficult  to  stain  than  the  clubs.  In  some 
cases  it  seems  to  branch.  The  filaments  can  rarely  be  seen  in 
the  rosettes  as  thej'  occur  in  the  suppurating  lesions. 

The  natural  habitat  of  this  fungus  is  said  to  be  on  certain 
plants.  According  to  Brazzola,  they  vegetate  on  the  grasses, 
chiefly  on  Hordeinu  murinum.  He  discovered  quantities  of 
the  fungi  between  the  vegetable  fibres  of  barley  which  were 
imbedded  in  the  gums  of  animals.  Johne,  Plana,  Bostroem 
and  others  have  found  it  on  the  awns  of  corn  which  were 
imbedded  in  the  tonsils  of  pigs  and  in  the  tongues  of  cattle. 
Mayo,  after  making  a  careful  study  of  this  disease,  states  that 
the  actinomyces  are  probably  a  degenerative  form  of  some 
fungus  which  grows  naturally  upon  food  stuffs  or  grain.  Bos- 
troem entertains  the  view  that  they  develop  exclusively  on 
grains,  particularly  on  the  awns  of  barley. 

The  period  of  incubation  is  not  known. 


304 


ACTINOMYCOSIS 


§  230.  Infection.  While  actinomycosis  is  an  infectious 
disease  it  does  not  seem  to  be  transmitted  directly  from  one 
animal  to  another.  Numerous  investigators  have  tried  to  pro- 
duce the  disease  by  inoculating  cattle,  calves,  sheep,  goats, 
pigs,  dogs,  cats,  rabbits  and  guinea  pigs  with  actinomycotic 
lesions.  The  results  have  almost  invariably  been  negative 
when  pus  was  used,  but  the  disease  has  developed  after  inocu- 


FiG.  72.     Head  of  a  steer  with  actinomycosis  of  the  loiver  jaw. 
( Photograph  ed  by  Hopkins ). 


lating  cattle  with  pieces  of  tissue  containing  the  fungus  in   its 
vegetating  state. 

It  is  believed  that  the  infection  occurs  in  susceptible 
species  by  the  introduction  of  the  fungus  on  food  stuffs.  The 
supposition  is  that  the  parasite  gains  entrance  to  the  living 
tissues  through  slight  wounds  of  the  mucous  membrane  of  the 
mouth  or  throat  and  perhaps  the  alveoli  of  diseased  teeth  or 
during  the  shedding  of  the  milk  teeth.  It  multiplies  and 
extends  from  the  points  of  entrance.      After  the  infected   awns 


SYMPTOMS 


305 


once  gain  lodgment,  especially  between  the  teeth,  they  are 
removed  only  with  difficulty.  The  favorite  points  for  the  act- 
inomyces  to  enter  the  tongue  is  on  the  upper  surface  midway 
between  the  dorsum  and  the  tip.  The  lungs  may  be  the  seat 
of  primary  infection  due  to  the  inhalation  of  the  fungus.  The 
disease  has  been  rarely  observed  primarily  in  the  udder  but 
frequently  in  the  subcutaneous  tissue  about  the  head.  In  man 
the  source  of  infection  is  more  obscure.  Man}-  cases  have 
been  reported  where  the  individuals  did  not  come  in  contact 
with  diseased  animals  and  were  not  occupied  in  agricultural 
pursuits  or  in  handling  grain  but  were  glaziers,  tailors  and 
various  shop  tenders.  There  are  a  few  cases  reported,  how- 
ever, where  the  circumstantial  evidence  points  to  direct  infec- 
tion from  diseased  animals. 

The  present  knowledge  of  this  fungus  indicates  that  it 
must  attain  to  a  certain  stage  or  period  in  its  development 
before  it  will  live  and  multiply  in  living  animal  tissues.  It 
has  been  observed  that,  as  a  rule,  cattle  become  infected  when 
they  are  kept  upon  dry  food. 

^  231.  Symptoms.  Actinomycosis  is  manifested  by  a 
firm  swelling  or  tumor  usually  situated  in  the  region  of  the 
head  or  throat.  It  is  first  recognized  as  d  slight  swelling  of 
the  affected  part  resembling  somewhat  the  result  of  a  bruise. 
It  is  stated  by  those  who  have  had  much  experience  with  the 
disease  that  many  cases  of  actinomycosis  seem  to  be  caused  by 
blows  or  injuries  received  while  struggling  in  stanchions. 
The  enlargement  gradually  increases  in  size.  It  is  ordinarily 
sharply  defined  from  the  surrounding  tissues. 

Upon  manipulation  the  tumor  feels  hard  and  dense.  In 
the  region  of  the  tliroat  it  may  be  fluctuating.  After  a 
variable  length  of  time,  the  tumor-like  mass  may  soften  in  one 
or  more  places,  rupture  and  discharge  a  rather  thick,  yellow- 
ish and  more  or  less  sticky,  purulent  substance.  The  dis- 
charge may  continue  or,  as  often  happens,  the  opening  heals 
temporarily  only  to  rupture  again.  The  discharge  often  takes 
place  into  the  cavity  of  the  mouth  or  throat.     Sometimes  the 


3o6 


ACTINOMYCOSIS 


neoplastic  tissue  increases  in  amount  until  it  gradually  forces 
its  way  through  the  opening,  resembling  somewhat  a  cauli- 
flower in  appearance.  The  actinomycotic  growth  frequently 
increases  rapidly  in  size  after  it  has  discharged.  In  later 
stages  the  teeth  may  become  ulcerated  and  loose. 

When  the  tongue  is  affected  the  animal  finds  it  difficult  to 
eat.  The  organ  is  swollen  and  in  advanced  cases  hangs  from 
the  mouth.     There  is  in  these  cases  profuse  salivation.     When 

the  pharynx  is  affected 
there  is  difficulty  in  swal- 
lowing and  when  the  larynx 
is  attacked  there  is  difficul- 
ty in  breathing.  In  this 
country  the  tumor  is  most 
frequently  seen  on  the  ex- 
ternal surface  of  the  jaw. 
It  is  stated  by  Salmon  that 
it  usually  begins  in  the 
connective  tissue  beneath 
the  skin  but  soon  extends 
to  the  bone,  which  it  pene- 
trates. Actinomycosis  of 
the  cervical  vertebrae  may 
cause  spinal  paralysis. 
When  the  lungs  are  at- 
tacked the  animal  may  present  the  appearance  of  one  suffering 
from  a  chronic  pulmonary  disease  such  as  tuberculosis. 

Actinomycosis  is  not  a  rapidly  fatal  disease.  Animals 
rarely  if  ever  die  from  its  immediate  effects.  The  length  of 
time  during  which  they  survive  depends  very  largely  upon  the 
location  of  the  tumor  and  the  rapidity  of  its  development.  If 
the  tumor  is  situated  where  it  does  not  interfere  seriously  with 
prehension,  mastication  or  swallowing  of  food  or  where  it  does 
not  occlude  or  press  upon  the  respiratory  passages  the  animal 
usually  survives  for  several  years.  When  death  occurs  it  is 
usually  due  to  inanition,  the  animal  being  unable  to  take 
sufficient   food,  although   the  drain   upon  the   system   by   the 


^^ 

1     V^-'-      •' 

'-  u.  ^ 

Fig.  73.  A  draiuing  of  a  very  young 
actinomycotic  growth.  A,  actino- 
inyces ;  B,  giant  cell ;  C,  surround- 
ing reactionary  zone. 


MORBID     ANATOMY 


307 


long  continued  discharge  of  pus  must  be  severe.  Mayo  reports 
several  cases  where  the  disease  was  watched  for  five  or  six 
years  and  where  it  would  possibly  have  continued  several  years 
more  had  not  the  animals  been  destroyed.  Most  animals  which 
become  affected  with  actinomycosis  are  either  destroyed,  treated 
or  slaughtered  for  beef  in  the  early  stages  of  the  disease. 


232.       Morbid     anatomy.       The 


new    actinomycotic 


>    \, 


V 


v\ 


Fi(;.  74.     A  c/ra?i.'i/ij>'  o/afi  ac/ifi07nyrolzcjazi.'. 

growths  have  in  or  near  their  centers  rosettes  of  the  ray  fungus 
surrounded  usually  by  giant  cells.  These  in  turn  are  sur- 
rounded by  tissue  consisting  principally  of  epithelioid  and 
spindle  shaped,  connective  tissue  cells,  among  which  giant 
cells  may  appear.  As  these  cells  increase  in  number  they 
press  against  the  surrounding  tissues,  thus  producing  the  hard 
and  dense  tumor-like  growths.  This  is  especially  true  when 
they  are  located  in  the  connective  tissue.  In  certain  other 
positions,  such  as  the  liver,  the  inflammatory  cells  are  sur- 
rounded by  a  fibrous  tissue  framework  which  gives  to  the 
lesion  a  honeycomb  appearance.  On  section  a  disagreeable 
"nutty"  odor  is  given  off  which  Mayo  considers  to  be  quite 
characteristic  of  the  di.sease.       The  outside  of  the    tumor    is 


3o8 


ACTINOMYCOSIS 


usually  composed  of  a  dense  layer  of  fibrous  connective  tissue. 
Extending  from  the  periphery  toward  the  center,  the  tissue 
becomes  less  dense  and  is  composed  largely  of  epithelioid  cells. 
In  the  softer  tissue  there  are  often  cavities  of  greater  or  less 
size  filled  with  a  viscid  purulent  substance  in  which  the  small, 
yellowish  granules  of  the  ray  fungus  can  be  found.  If  this 
pus  is  spread  in  a  thin  layer  on  a  smooth  surface  granules  com- 
posed of  the  "ray  fungus"  can  often  be  seen  with  the   unaided 


Fig.  75.     Photograph  of  a  section  through  an  actinomycotic  jaw  :  (a) 
tooth,  (d)  done,  (c)  actinomycotic  tissue. 

eye.  These  pus  cavities  are  usually  connected  with  each  other 
by  small  sinuses  but  sometimes  they  are  separated  by  bands  of 
fibrous  tissue. 

If  the  disease  is  in  the  bone,  usually  in  the  head,  as  it  is 
when  the  specific  organism  gains  entrance  and  begins  to  grow 
in  the  interior  of  the  jaw,  the  bone  tissue  about  the  organism 
becomes  in  places  disintegrated  and  absorbed  and  pockets  are 
formed  containing  the  fungus.  While  the  interior  of  the  bone 
is  being  broken  down  and  absorbed  by  the  action    of  the  acti- 


MORBID    ANATONV 


309 


iiomycotic  growth  within,  its  diameter  is  being  increased  by 
the  deposition  of  new  tissue  until  it  may  become  several  times 
its  normal  size. 

The  lesions  spread  in  most  cases  by  gradual  invasion  of 
the  tissues  surrounding  the  infected  point.  At  the  seat  of 
infection,  minute,  inflammatory  points  appear,  which  extend  at 
their  periphery  and  unite  to  form  larger  areas  of  diseased 
tissue.  These  masses  tend  to  extend  in  one  direction  and  to 
heal  in  another,   leaving  behind  bands  of    cicatricial    tissue. 


Fig.   76.     Actinomycosis  of  the  upper  ja7c.    {Photoiiraphed  by  Hopkins) . 


The  process  usually  differs  widely  from  that  of  a  simple 
inflammation.  In  its  progress  the  disease  shows  no  preference 
for  structures  but  invades  one  tissue  after  another  so  that  all 
may  be  involved  alike. 

The  lymphatics  show  no  constant  tendency  to  become 
involved.  Metastasis  occurs  in  a  very  small  proportion  of  the 
cases.  When  it  does,  as  reported  by  Ponfick,  large  areas  may 
be  simultaneously  affected.      He  reports  a  case  in   the  human 


3IO 


ACTINOMYCOSIS 


subject  in  which  the  left  jugular  vein  was  perforated  by  a  mass 
of  the  fungi  resulting  in  the  formation  of  actinomycotic  infarcts 
in  the  lungs,  spleen,  brain,  and  heart. 

In  cattle,  actinomycosis  usually  appears  in  one  or  more  of 
the  following  locations. 

1.  /;/  the  inaxillary  bones.  Here  it  generally  results  in 
large  tumor-like  growths.  Actinomycosis  of  the  jaw  usually 
commences  with  flat  granulation  of  the  gums  and  mucous 
membranes  in  the  neighborhood  of  the  teeth  and  spreads 
finally  to  the  medullary  tissues  of  the  bone  and  to  the  perios- 
teum, soon  giving  rise  to  the  osseous  tumor.  From  the  maxil- 
lary bone  the  disease  may  advance  either  to  the  subcutaneous 
connective  tissue  and  the  skin  or  to  the  oral  cavity  in  the 
direction  of  the  molar  teeth,  which  become  displaced. 

2.  In  the  ton  one.  When  the  lesions  appear  in  this  organ 
the  disease  takes  the  form  of  an  indurating  glossitis.  The 
tongue  becomes  thickly  sprinkled  with    round    or  oval,    hard, 


Fig.  77.    Actinomycosis  of  the  tongue,  '^zuooden  tongue 
by  Hop/cins). 


[P/io  tog  rap  tied 


fibrous  nodules  which  finall}'^  become  purulent  or  chalky  at  the 
center.  Around  these  there  is  a  considerable  increase  of  con- 
nective tissue  which  leads  to  the  atrophy  of  the  muscle  fibers. 


MORBID    ANATOMY  31I 

Upon  section  the  tongue  is  found  to  be  hard  and  often  gritty. 
The  indurated  tongue  is  often  eroded  from  friction  and  various 
deformities  of  this  organ  are  reported. 

3.  1)1  the  pharynx.  Here  the  disease  usually  takes  the 
form  of  soft  polypoid  or  fungoid  nodules  or  lumps  with  a 
smooth  surface  and  short  peduncle.  These  nodules  vary  in 
size  often  reaching  that  of  a  goose's  ^'g'g.  These  polypoid 
growths  may  cause  great  difficulty  in  swallowing  and  likewise 
interfere  with  respiration.  Tumors  of  this  kind  may  form  in 
the  esophagus  or  trachea.  Rarely  actinomycotic  growths 
occur  at  other  places  in  the  alimentary  tract.  There  are  some 
cases  in  which  the  lesions  are  not  restricted  to  the  digestive 
tract. 

4.  1)1  the  skin  and  subcutaneous  tissue.  The  lesions  of 
the  skin  and  subcutis  are  found  chiefly  on  the  head  and  neck. 
They  usually  consist  of  firm  nodules  from  the  size  of  a  hazel 
nut  to  that  of  a  man's  fist  or  even  larger.  Sometimes  these 
nodules  are  pedunculated  and  at  others  they  are  attached  to 
the  skin  by  a  broad  base.  Instead  of  the  hard  tumor  there 
may  occur  soft  granular  fungoid  proliferations  covered  with  a 
brown  crust  or  with  a  purulent  secretion.  At  other  times 
minute  nodules  appear  in  these  proliferations  and  the  .skin 
becomes  thickened  and  indurated.  However,  the  skin  lesions 
may  become  very  large.  In  this  organ,  the  disease  may  be 
either  primary  or  secondary. 

5.  In  the  lymph  glands.  Actinomycosis  often  appears  in 
the  lymph  glands  of  the  head,  larynx  and  pliarynx.  The 
parotid  and  submaxillary  glands  are  sometimes  involved  as 
secondary  infections.  It  is  reported  that  the  sub-parotid 
glands  are  most  frequently  affected. 

6.  hi  the  lu)io-s.  The  lesions  in  the  lungs  vary.  They 
may  consist  of  firm,  .somewhat  yellowish  nodules  which  event- 
ually become  calcareous  in  their  center  and  vary  in  size  from 
mere  specks  to  that  of  a  pea.  This  form  is  spoken  of  as 
miliary  actinomycosis.  In  the  second  form  the  actinomycotic 
foci  .soften  and  become  filled  with  a  gray  mucopurulent  fluid. 


312 


ACTINOMYCOSIS 


The  lesion  may  spread  to  the  pleurae  and  even  reach  to  the 
surface  of  the  bod}-  by  penetrating  through  the  thoracic  wall. 
The  bronchial  glands  and  the  mucosa  of  the  air  passages  may 
also  become  affected. 

7.  hi  other  organs.  Actinomycosis  has  been  reported 
rarely  as  attacking  the  udder,  spermatic  cord,  brain,  spleen, 
liver,  muscle,  diaphragm,  peritoneum,  inguinal  glands,  vagina, 
uterus  and  cervical  vertebrae. 

Assmann  has  recently  summarized  the  literature  on  the 
dissemination  of  the  lesions  and   has  concluded    that   general- 


FiG.  78.     r/iotograph  0/ a  portion  of  a  coic's  tting,  shoicing  area  of 
acti)wniycotic  tissue  surrounded   by  a    wall  of 
connective  tissue.     Natural  size. 


ized  actinomycosis  is  not  rare  in   occurrence.      He  gives  a  de- 
tailed description  of  eleven  cases  in  cattle  and  hogs. 

It  is  stated  by  Salmon  that  in  England  the  disease  ap- 
pears most  often  in  the  tongue,  in  Denmark  the  soft  parts  of 
the  head  are  affected  most  frequently,  while  in  some  parts  of 
Germany  it  is  most  frequently  found  in  the  pharynx.  In  the 
United  States  it  usually  appears  in  the  lower  jaw.  In  man  as 
in  cattle,  the  appearance  of  the  lesions  varies  according  to  the 
part  infected.  In  some  cases  the  lesions  closely  resemble 
those  of  chronic  inflammation  but  in  others,  such  as  the  liver 


DIFFERENTIAL    DIAGNOSIS  313 

or  skin,  they  are  often  characteristic.  In  the  lungs  the  lesions 
have  frequently  been  mistaken  for  tubercle.  Usually  the  dis- 
ease affects  the  head  and  if  the  maxillary  bones  are  attacked 
the  teeth  are  usually  lost. 

Actinomycosis  in  swine.  Actinomycosis  appears  in  this 
species  in  the  lower  jaw,  larynx,  lungs,  wounds  caused  by 
castration,  in  the  mammary  gland,  muscles  and  bones.  The 
character  of  the  lesions  does  not  differ  to  any  marked  extent 
in  swine  from  those  in  cattle  or  man.  In  case  of  bone  infection 
purulent  cavities  and  sinuses  are  formed  in  which  the  yellow 
granules  of  the  fungus  occur.  It  is  reported  that  occasionally 
pigs  suffer  from  generalized  actinomycosis.  Duncker  has 
found  in  the  muscles  of  the  pig  a  variety  of  the  ray  fungus 
which  has  been  called  Actinomycosis  mnscolorum  suis,  to  dis- 
tinguish it  if  possible  from  the  bovine  species.  Its  relation  to 
the  actinomycosis  bovis  has  not  been  clearly  determined.  It 
is  reported  to  have  been  found  frequently. 

Actinomycosis  in  Iiorscs  and  sliccp.  In  the  horse,  acti- 
nomycosis of  the  bones,  tongue,  trachea,  spermatic  cord  and 
submaxillary  glands  has  been  observed.  The  disease  is  re- 
ported to  have  been  mistaken  for  glanders.  The  affection 
known  as  scirrhous  cord  seems  to  be  due  in  rare  cases  to  an 
infection  by  the  ray  fungus.  One  such  case  has  occurred  in 
the  clinic  of  this  institution.  A  very  few  cases  of  this  disea.se 
have  been  reported  in  sheep,  the  lesions  being  restricted  to  the 
lungs  or  muscles. 

§  233.  Differential  diagnosis.  In  cattle  actinomycosis 
is  to  be  differentiated  (i)  from  tuberculosis,  especially  of  the 
lungs,  glands  of  the  throat,  head  and  the  udder,  (2)  various 
forms  of  glossitis,  polypoid  growths  in  the  pharynx,  fibroma, 
.sarcoma  and  osteosarcoma  of  the  jaw,  parotitis  and  cellulitis. 
The  writer  has  seen  a  few  cases  of  bacterial  infection  of  the 
maxillary  glands  giving  rise  to  the  formation  of  large  quanti- 
ties of  caseous  matter  which  caused  swelling  and  firmness 
suggestive  of  actinomycotic  tumors.  In  one  instance  a  speci- 
men reported  to  l)e  actinomycosis  was  examined  and  found  to 


314  ACTINOMYCOSIS 

contain  a  piece  of  bone  about  three  inches  long  which  had 
become  wedged  between  the  teeth  and  cheek  and  surrounded 
by  inflammatory  tissues.  Frohner  calls  attention  to  conta- 
gious diseases  as  possibly  being  mistaken  for  this  disease. 

The  affection  recently  described  by  Lignieres  as  actitio- 
bacillosis  is  to  be  distinguished  from  actinomycosis  of  the  skin. 
It  is  thought,  however,  by  many  workers  that  actinobacillosis 
is  a  variety  of  actinomycosis. 

In  making  a  positive  diagnosis  of  actinomycosis  it  is 
necessary  to  make  a  microscopic  examxination  of  some  of  the 
diseased  tissue  or  of  the  discharged  pus  in  which  the  ray 
fungus  may  be  found  if  the  disease  is  actinomycosis.  It  is 
impossible  to  obtain  this  positive  proof  from  the  living  animal 
when  the  disease  is  situated  in  the  internal  organs.  With 
these  it  is  necessary  to  depend  largely  upon  the  history  and 
general  condition  of  the  animal.  In  preparing  the  discharged 
pus  for  a  microscopic  examination  it  is  usually  sufficient  to 
crush  one  or  more  of  the  yellowish  granules  between  a  slide 
and  cover-glass.  It  is  of  advantage  to  wash  it  with  a  dilute 
solution  of  caustic  soda  to  clear  away  the  pus  cells.  The 
rosettes  are  easily  recognized  with  a  low  magnification. 

In  man,  actinomycosis  is  to  be  differentiated  from  certain 
forms  of  tuberculosis  and  the  Madura  foot  disease  which  was 
described  by  Carter,  in  i860,  as  a  "  fungus  disease. "  This 
is  a  chronic,  locally  spreading  inflammation  of  the  foot,  rarely 
of  the  hand,  causing  the  destruction  of  the  part  involved  and 
giving  rise  to  a  great  overgrowth  of  connective  tissue.  My- 
cetoma almost  invariably  attacks  the  hand  or  foot  and  accord- 
ing to  Carter  there  are  no  secondary  deposits  in  the  viscera. 
In  actinomycosis  the  extremities  are  rarely  attacked  and  the 
viscera  are  often  the  seat  of  the  disease  ;  further  the  mycetoma 
is  a  disease  of  hot  climates  while  actinomyco.sis  is  a  disease  of 
the  temperate  latitudes.  The  fungus  of  the  two  affections 
seem  to  be  closely  related  but  as  yet  their  identity  has  not 
been  established. 

^  234.  Specific  treatment.  The  investigations  of 
Thomas.sen,    Nocard,   and  Norgaard  and  the   experience  of  a 


SANITARY    CONSIDERATIONS  315 

large  number  of  veterinarians  have  proved  verj^  conclusively 
the  specific,  curative  effect  of  iodide  of  potassium.  According 
to  Salmon  the  iodide  of  potassium  is  given  in  doses  of  from 
1.5  to  2.5  drams  dissolved  in  water  and  administered  in  a 
drench,  once  a  day.  The  dose  should  var}'  somewhat  with  the 
size  of  the  animal  and  with  the  effects  that  are  produced.  If 
the  dose  is  sufficiently  large  there  appear  signs  of  iodism  in  the 
course  of  a  week  or  ten  days.  The  skin  becomes  scurvy,  and 
the  eyes  moistened.  There  is  nasal  catarrh  and  loss  of  appe- 
tite. When  these  symptoms  appear  the  medicine  may  be 
suspended  for  a  few  days  and  afterwards  resumed  in  the  same 
dose.  The  cure  requires  from  three  to  six  weeks'  treatment. 
Some  animals  do  not  improve  with  the  administration  of 
iodide  of  potassium  and  these  are  generally  the  ones  which 
show  no  signs  of  iodism. 

If  there  is  no  sign  of  improvement  after  the  animals  have 
been  treated  four  or  five  weeks  and  the  medicine  has  been 
given  in  as  large  doses  as  appears  desirable,  it  is  an  indication 
that  the  particular  animal  is  not  susceptible  to  the  curative 
effects  of  the  drug  and  the  treatment  should  be  abandoned. 

It  is  not,  however,  advisable  to  administer  iodide  of  potas- 
sium to  milch  cows,  as  it  will  considerably  reduce  the  milk 
secretion  or  stop  it  altogether.  Furthermore,  a  great  part 
of  the  drug  is  excreted  through  the  milk  making  it  unfit  for 
use.  It  should  not  be  given  to  animals  in  advanced  pregnancy, 
as  there  is  danger  of  producing  abortion. 

v^  235.  Sanitary  considerations.  The  literature  upon 
this  subject  is  largely  to  the  effect  that  actinomycosis  is  rarely 
if  ever  either  contagious  or  infectious  in  the  sense  that  it  can 
be  transmitted  from  one  animal  to  another  or  from  one  of  the 
lower  animals  to  man.  There  seems  to  be  no  indisputable  case 
on  record  of  such  a  transmission,  although  a  few  cases  are 
very  suggestive.  It  is  the  opinion  of  most  pathologists  that 
when  the  disease  is  restricted  to  small  tumors  and  these  are 
localized,  that  the  affected  parts  should  be  destroyed  but  the 
remainder  of  the  carcass  may  be  used  for  human  consumption. 

In  Bulletin   No.    2,   of  the   Board  of  Live  Stock  Commis- 


31 6  ACTINOMYCOSIS 

sioners  of  Illinois,  published  in  1891,  is  the  report  of  the  some- 
what famous  trial  in  the  Peoria  county  circuit  court  of  the  case 
of  J.  B.  Greenhut  et  al.  vs.  John  M.  Pearson  et  al.  to  recover 
damages  for  the  rejection  and  destruction  of  certain  actinomy- 
cotic cattle,  in  which  is  given  the  testimony  of  a  large  number 
of  distinguished  veterinarians  and  sanitarians  concerning  the 
wholesomeness  of  the  meat  of  cattle  affected  with  this  disease. 
Although  at  that  time  there  was  a  strong  popular  sentiment 
against  the  use  of  such  animals,  the  jury  after  a  forty  hours' 
consideration  reported  their  inability  to  agree  and  were  dis- 
charged by  the  court.  The  most  conspicuous  feature  of  this 
evidence  was  the  inability  of  the  witnesses  to  produce  satis- 
factory evidence  of  the  communicability  of  the  disease  from 
animal  to  man.  This  evidence  did  much  to  show  that  the 
danger  from  this  disease  in  eating  meat  of  affected  animals  was 
after  all  a  matter  of  opinion,  fear  or  sentiment  rather  than  a 
demonstrated  fact.  Mayo,  in  his  bulletin  upon  the  subject, 
states  that  there  is  no  danger  of  persons  contracting  this  dis- 
ease from  eating  the  flesh  of  affected  animals  provided  the 
visibly  diseased  portions  are  removed. 

RRFERKNCKS 

1.  BOSTROEM.  Untersuchungen  iiber  das  Aktinomj^kose  des  Meu- 
schen.  Beitrag.  ziir  path.  Anat.  11.  zur  allge.  Pathologic,  Bd.  IX 
(1891),  S.  I. 

2.  Israel.  Neue  Beobachtungen  auf  den  Gebeite  des  Mykosen 
des  Menschen.      Virchow's  Archiv,  Bd.  LXXVI  (1878),  S.  11. 

3.  Mavo.  Actinomycosis  bovis  or  "lumpy-jaw."  Bulletin  No. 
jS,  Kansas  State  Agric.  Exp.  Station,  1892. 

4.  Moore  Actinomycosis  mistaken  for  tuberculosis  at  post- 
mortem following  the  tuberculin  test.  A»i.  I'et.  Revicic,  Vol.  XXX 
(1906),  p.  181. 

5.  NocARD.  Notes  sur  l'actinom3'cose  des  animaux.  Rccueil  de 
Med.  VHer.     Vol.  LXIX  (1892),  p.  167. 

6.  Salmon.  Treatment  of  lumpy-jaw  or  actinomycosis  in  cattle. 
Bulletin  No.  2,  U.  S.  Bureau  of  Animal  Industry ,  1893. 

7.  vSalmon.  Actinomycosis  or  lumpy-jaw.  Annual  Report, 
Bureau  of  Aninial  Industry,  1893-4,  p.  88. 


INFKCTIOUS    DISEASES 


317 


8.  WoLFK  UNI)  IsRAKi..     UeberReinculturdes   Actinomyces  und 
seine    Uebertrag1)arkeit     auf     Tliiere,        Virc/i.      Arch       Bd'     XXVI 

(1891),  vS.    II. 

9.  Wright.     The  biology  of  the  microorganism  of  actinomycosis. 
The  Jour.  0/ Med.  Research,  Vol.  XIII  (1905),  p.  349. 


ACTIXOBACILLOSIS. 

§236.  Characterization.  Actinobacillosis  is  described 
as  an  infectious  disease  of  cattle,  characterized  by  its  clinical 
resemblance  to  actinomycosis.  It  is  caused  by  an  organism 
which  "resembles,  in  marked  degree,  the  bacterium  of  Fowl 
Cholera."  It  arranges  itself  in  the  tissues  in  "rosette"  or 
ray-like  forms.  It  is  thought  by  some  workers  to  be  a  variety 
of  actinomycosis.  It  is  described  as  an  independent  and  dis- 
tinct disease. 

§237.  History.  Lignieres  and  Spitz  described,  in  1902, 
a  disease  in  cattle  resembling  actinomycosis  but  which  was 
caused  by  a  bacterium.  Until  1900-01  this  affection  was  not 
differentiated  from  actinomycosis.  Nocard,  in  1902,  identified 
the  disease  in  France.  In  [904,  Higgins  described  four  cases 
in  Canada.  These  appear  to  be  the  only  records  we  have  of 
this  affection. 

§  238.  Geographical  distribution.  It  is  reported  by 
Lignieres  and  Spitz  to  be  epizootic  in  Argentine  Republic. 
It  has  been  described  in  France,  and  in  Canada. 

§  239.  Etiology.  This  disease  is  caused,  according  to 
its  investigators,  by  a  bacterium  which  arranges  itself  in  the 
tissues  in  a  rosette  or  ray-like  appearance.  It  is  aerobic, 
facultative  anaerobic,  non-motile  and  of  a  variable  size,  rang- 
ing between  i.o  and  1.8  /<  in  length  and  from  0.4  to  0.6  //  in 
breadth.  According  to  Higgins,  it  has  a  distinct  polar  arrange- 
ment of  the  protoplasm  as  observed  in  the  hanging  drop  prep- 


3l8  ACTINOBACILLOSIS 

aration.  It  stains  with  the  ordinary  aniUne  dyes.^'  It  does 
not  take  the  Gram  stain. 

In  the  fresh  tissues  or  in  sections  it  appears  in  granules 
the  same  as  in  actinomycosis. 

The  actinobacillose  is  virulent  for  guinea  pigs  and  rab- 
bits.     When  inoculated  into  the   abdominal   cavity  with  pure 


% 


Fig.  79.     A  photograph  of  a  section  of  a    tuuior  stained  by   Gram's 
tnethod  but  not  fully  decolorized.      X  about  r, 000.    [After  Higgins). 


*Higgins  recommends  the  Romanowsky  stain  as  modified  by  Dut- 
ton'^and  Todd  for  sections  or  preparations  from  pus.  The  formula  for 
the  stain  and  method  for  its  use  are  as  follows : 

Stain:     Eosin,  aqueous  solution i  part 

Borrell's  Blue i     " 

Water 8  parts 

Mix  just  before  using  and  filter.  Suspend  the  preparations  (sections 
fixed  to  the  slide)  upside  down  on  the  stain  to  saturate  them  from 
below,  to  avoid  precipitate.  Stain  in  this  solution  for  thirty  minutes. 
Wash  thoroughly  in  water,  then  in  a  10%  solution  of  tannic  acid,  which 
will^brighten  the  color,  and  again  wash  in  water.  Dehydrate  in  alcohol, 
clear  and  mount  in  xylol  balsam.  The  stain  as  above  prepared  spoils 
quickly. 


MOkHID    ANAT<)!\IY  -^ig 

cultures  guinea  pigs  die  in  from  nineteen  to  thirty-one  days 
( Higgins)  of  generalized  actinobacillosis.  These  are  reported 
to  be  characteristic  and  different  from  those  of  any  of  the 
other  observed  infective  agents.  According  to  Higgins, 
"Small  pearly-white  nodules  appear  just  beneath  the  peri- 
toneal and  pleural  membranes,  varying  from  i.o  to  5.0  mm.  in 
diameter.  The  liver  presents  lesions  throughout  its  subtance, 
the  surface  being  mottled.  The  spleen  .shows,  usually,  a 
varying  number  of  nodules.  The  great  mesenteric  fold  of  the 
omentum  has  in  every  instance  been  the  seat  of  extensive 
lesions.  The  kidneys  present  nodules  beneath  their  serous 
covering,  but  none  have  been  observed  in  the  substance  of  the 
organ.  The  stomach  and  intestines  usually  present  nodules 
on  their  serous  surfaces,  varying  from  i.o  to  0.5  mm.  in  dia- 
meter. ' '  There  are  other  lesions  such  as  ulcers  in  the  stomach, 
nodules  in  the  heart  and  pericardium.  Subcutaneous  inocula- 
tions are  usually  followed  by  similar  lesions. 

Rabbits  are  said  to  react  the  same  as  guinea  pigs.  Nocard 
found  an  intravenous  injection  fatal  to  dogs  in  24  hours.  In 
horses  a  local  abscess  resulted  which  healed  rapidly. 

The  method  of  infection  has  not  been  fully  explained,  but 
it  is  supposed  that  the  organisms  are  taken  with  food  as  in 
cases  of  actinomycosis. 

The  organisms  are  .said  to  agglutinate  in  .serum  of  animals 
affected  with  actinobacillosis. 

It  is  destroyed  in  10  minutes  at  62°  C.  It  grows  best  at 
incubator  temperature  (37°  C).  It  is  not  rapidly  destroyed 
by  freezing. 

i^  240.  Symptoms.  They  do  not  appear,  in  cattle,  to 
be  differentiated  from  those  of  actinomycosis. 

§  241.  Morbid  anatomy.  The  lesions  are  very  similar 
to  those  of  actinomycosis.  The  location  of  the  affected  parts 
varies.  Lignieres  describes  it  as  attacking  the  skin,  lymphatic 
glands,  tongue,  pharynx,  mammary  glands,  the  viscera  and 
bones.  The  tissue  changes  appear  to  be  an  infiltration  of  puru- 
lent material,   and  the  new  formation    of  connective    ti.ssue. 


320  ACTIONOBACILLOSIS 

The  skin  is  often  affected.  In  the  single  specimen  which  the 
writer  has  had  an  opportunity  to  study,  the  ray-like  arrange- 
ment of  the  organism  and  the  tissue  immediately  surrounding 
it,  could  not  be  easily  distinguished  from  a  section  of  actin- 
omycosis. 

ij  242.  Differential  diagnosis.  Actinobacillosis  is  to  be 
differentiated  from  actinomycosis,  tuberculosis,  perhaps  cer- 
tain parasitic  diseases  of  the  skin,  and  localized  bacterial 
infections. 

The  diagnosis  is  made  from  the  various  locations  of  the 
lesions.  The  more  important  of  these  is  the  apparent  selec- 
tion of  the  skin.  The  examination  of  the  fresh  pus  does  not 
reveal  the  yellow  granules  as  observed  in  actinomycosis  but 
when  squeezed  between  two  cover-glasses  they  are  said  to  be 
distinct.  The  actinobacillosis  does  not  take  the  gram  stain,  it  is 
infectious  for  guinea  pigs  and  rabbits,  and  it  is  readily  cultiva- 
ted on  artificial  media.  It  appears  to  be  transmitted  more 
often  in  cattle  by  cohabitation  than  actinomycosis. 

The  differentiation  from  any  parasitic  trouble  is  made  by 
the  finding  of  the  animal  parasite.  The  nature  of  the  lesions 
and  the  finding  of  tubercle  bacteria  in  the  discharge  by  micro- 
scopic examination,  or  by  producing  tuberculosis  in  guinea 
pigs  by  inoculations,  would  differentiate  it   from   tuberculosis. 

§  243.  Prevention.  As  the  natural  habitat  of  <?r/'/;z(?(^<3'- 
cillose  is  not  known,  the  source  of  infection  is  undetermined 
and  consequently  effective  preventive  measure  are  not  known. 
The  fact  that  it  seems  to  spread  from  infected  to  healthy  cattle 
necessitates  the  isolation  of  the  infected.  It  is  more  desirable 
when  possible  to  separate  the  well  from  the   infected   animals. 

REFERENCES. 

1.  HiGGiNS.  Actinobacillosis.  Bulletin  No.  /,  Biological  Lab- 
oratory, Department  of  Agriculture,  Dominion  of  Canada,  1904.  Also 
Proceedings  Amer.  Vet.  Med.  Asso.,  1904. 

2.  Lignib;res  and  Spitz.  Actinobacillose.  Contribution  a 
V  Hude  des  affections  connues  sous  le  nom  d'actinomycose.  Buenos  Aires> 
1902. 


i.ep:ches 


32  r 


3.  LiGNiKKics  AND  Spitz.  Actinohacillose.  Rccueil  de  IMedicine 
\''Hcrinaire,  1903. 

4-  NoCARi).  Actiiiobacillose  der  Znnj<e.  A/Z/r.  o'^.?  Vet.  Med. 
Berlin,  Bd.  I.VI  (1903),  p.  695,    (abstract). 


LEECHES. 

Syjionyms.  Summer  sore  ;  leeching  ;  barsati,  barsdti,  bar- 
sattee,  barsatti,  baiisette,  bursafi,  bursatie,  burusaltec,  biirsatti, 
bursaidee,  bursaiitie,  bursautlie,  bursotlee  and  bunisatitice.  These 
names  have  been  derived  from  the  Indian  word  burns  or 
bursaf,  meaning  rain  or  rain  sore,  it  having  been  supposed  that 
the  malady  was  associated  with  the  rainy  season. 

§244.  Characterization.  "  Leeches  "  or  "  leeching  " 
is  an  infectious  disease  quite  prevalent  among  the  horse  kind 
in  Florida  with  lesions  localized  on  the  skin  or  the  muco.sa  of 
the  head.  It  is  thought  by  many  that  this  affection  is  identical 
with  the  disease  known  as  bursattee*  in  India. 

§  245.  History.  Neal  of  Florida  described  this  disease 
as  affecting  horses  and  cattle.  He  believes  it  to  be  peculiar  to 
that  section,  where  he  states  it  is  common  and  very  fatal  to 
horses  and  mules.  There  are  hundreds  of  ponds  in  the  central 
portion  of  the  state  around  the  margins  of  which  there  is 
usually  a  belt  of  grassy  prairie,  water  grass  and  water  lilies. 
Into  these  grassy  places  the  horses,  mules  and  cows  often  go 
during  the  summer  and  feed  all  day  in  the  water.  He  adds, 
"after  a  varying  exposure  to  the  influence,  or  whatever  it  may 
be  called,  of  the  'pond,'  a  slight  lump  or  elevation  of  the  skin 
may  be  found  on  some  part  of  the  body  that  has  been  sub- 
merged. To  the  touch  it  will  feel  as  if  a  grain  of  shot  were 
lodged  beneath  the  skin.  In  eight  or  ten  days  the  skin 
sloughs  olT  centrally   over  this  hard  spot,   leaving  a  bloody, 

*It  seems  to  be  true  that  an  entirely  different  affection  is  known  by 
the  same  name  in  the  northern  portion  of  the  United  States.  The  term 
"Leeches"  is  also  applied  to  the  condition  following  the  invasion  of  ths 
liver  fluke  [Fascio/a  hef>atica). 


322  LEECHES 

bruised-like  surface.  This  rapidly  grows  in  size  till  in  a  few 
weeks  there  is  a  raw  surface  from  four  inches  to  a  foot  square. 
This  oozes  blood  and  serum  and  no  pus.  An  examination 
will  usually  show  a  mass  of  yellow,  gritty  growth,  coral-like 
in  shape,  embedded  in  a  mass  of  bruised,  bloody  tissue,  dark 
incolor  with  the  edges  roughened,  elevated  above  the  skin,  and 
the  skin  decaying  at  the  outside  of  the  ulcer.  The  leech 
invades  almost  an}?^  tissue,  but  seems  most  common  on  the  legs, 
abdomen  and  sides.  Occasionally  it  is  found  in  the  head. 
The  invaded  tissues  decay  slowly  and  apparently  without  pain. 
I  have  seen  hoofs  cut  off,  the  abdomen  opened,  the  eyes  eaten 
out  and  the  teeth  destroyed." 

In  this  country  the  disease  has  not  attracted  very  much 
attention,  nor  has  it  been  considered  of  much  economic  import- 
ance. An  explanation  for  this  may  be  offered  on  account  of 
its  seemingly  non-contagious  character  and  because  it  has  been 
thought  to  be  confined  to  comparatively  limited  areas,  and 
because  the  animals,  although  infected,  may  be  utilized  for 
some  purposes.  On  account  of  the  chronic  course  of  the  dis- 
ease the  affected  animals  are  often  killed  from  a  sentiment  of 
mercy  before  the  disease  can  terminate  fatally. 

Although  this  affection  presents  many  points  of  similarity 
to  the  one  found  in  India,  the  question  of  their  complete  iden- 
tity ought  to  be  held  in  abeyance  until  a  more  thorough  inves- 
tigation can  be  made. 

In  a  recent  publication,  Dawson,  of  the  Florida  Experi- 
ment Station,  states  "that  'leeches'  or  bursattee  is  a  common 
disease  in  Florida,  which  manifests  itself  in  the  formation  of 
tumor-growths  which  have  some  of  the  characters  of  actinomy- 
cotic tumors.  Its  structure  is  fibrous,  and  contains  many 
sinuses,  which  discharge  a  bloody,  'honey-like'  fluid.  It  is  a 
fatal,  infectious  disease,  which  has  its  origin  in  the  skin  and 
finally  penetrates  all  the  tissues.  Here  and  there  in  the  tumor 
tissue  yellow  bodies  with  root-like  projections  may  be  found. 
These  bodies  are  called  'leeches'  by  the  natives.  They  consist 
of  the  mycelia  of  the  fungus  which  causes  the  disease.  The 
only  remedy  is  the  complete  removal  of  the    tumor    and   adja- 


HISTORY  323 

cent  tissue  at  once.  The  application  of  caustics  and  disinfect- 
ants makes  matters  infinitely  worse,  as  they  stimulate  the 
tissues  to  renewed  growth-activity.  In  Florida  the  disea.se 
affects  only  the  genus  equinus." 

In  1896,  some  of  the  diseased  tissue  from  cases  of  this 
affection  in  Florida,  were  sent  to  the  Bureau  of  Animal  Indus- 
try for  investigation.  They  were  studied  by  Fish,  who  made 
an  extended  report  on  the  results  of  his  findings.  He  also 
gave  a  very  complete  review  of  the  literature. 

Hodgson,  in  1853,  referred  to  the  sores  as  cancerous  ulcers 
and  Hart,  in  1872,  was  strongly  inclined  to  pronounce  it 
cancer,  although  he  could  not  confirm  this  view  structurally 
by  microscopic  examination  of  the  tissue.  It  seems  to  be 
generally  accepted  that  the  disease  is  peculiar  to  the  Tropics, 
but  cases  have  been  reported  in  Kansas  and  Minnesota  in  the 
United  States,  not  only  during  the  summer  months,  but  when 
the  thermometer  registered  below  zero.  We  might  also  expect 
that  the  disease  would  exist  in  Mexico  and  Central  and  South 
American  countries,  where  the  conditions  of  temperature  and 
moisture  are  favorable. 

Reports  show  that  a  high  temperature  is  essential  for  the 
development  of  the  disease,  although  exceptional  cases  are 
noted  as  occurring  during  the  cold  season.  Moisture  does  not 
seem  to  be  necessary,  since  man}'^  cases  develop  when  the  sea- 
son is  dry.  It  is,  however,  an  important  factor.  Statistics 
show  that  cases  are  more  numerous  and  that  the  disease 
assumes  a  more  aggravated  form  during  the  wet  season. 

In  India,  native  as  well  as  foreign  bred  horses  are  sus- 
ceptible, but  according  to  some  writers,  none  of  the  other 
equine  species  is  affected. 

In  the  United  States  mules  and  cattle  are  said  to  develop 
it,  but  not  so  readily  as  the  horse.  Outbreaks  among  cattle 
are  comparatively  rare.  Thin-skinned  animals  are  more  sus- 
ceptible than  thick-skinned  ones.  Some  discrepancy  of 
opinion  exists  as  to  the  kind  of  horses  most  likely  to  take  the 
disease  (assuming  that  bursattee  and  leeches  are  similar). 
Neal  states  that    only    horses   of   good   blood    leech,    and   the 


324  LEECHES 

Cuban  and  Texan  ponies  are  as  a  rule  exempt.  Anderson 
states  that  it  is  the  coarsely  bred  and  hard-worked  horses  that 
are  the  most  susceptible.  The  well-bred  ones,  having  the  ad- 
vantage of  good  hygienic  surroundings,  rarely  contract  it. 

§  246.  Geographical  distribution.  Bursattee  has  been 
reported  from  Bunnah  and  Hindoostan.  It  is  thought  that 
the  prevalence  of  the  disease  is  associated  with  the  principal 
river  systems  of  India.  In  the  hilly,  rocky  and  consequently 
drier  districts  there  is  a  very  noticeable  diminution  or  absence 
of  it. 

Outside  of  India  there  seem  to  have  been  no  cases  of  this 
malady  reported  except  in  the  United  States,  unless  upon  fur- 
ther investigation  certain  mycotic  diseases  which  have  been 
described  in  Europe  should  prove  to  be  identical  with  it. 

Lyford  (1866)  reported  it  in  Minnesota,  Anderson,  (1889) 
in  Kansas  and  Alabama,  and  Neal  ^1887)  and  Bitting  (1894) 
in  Florida.  The  latter  writer  states,  that  it  is  "now  known 
all  over  the  United  States  except  in  that  region  lying  east  of 
the  Alleghany  mountains  and  north  of  the  Potomac  river."  A 
few  cases  have  been  presented  for  treatment  in  the  clinic  of  the 
New  York  vState  Veterinary  College. 

-^  247.  Etiology.  A  summary  of  the  literature  shows 
that  among  the  old  theories  "leeches"  was  believed  to  be  a 
blood  disease  in  many  ways  not  unlike  syphilis,  scrofula  and 
farcy.  The  "fly  theory"  of  the  causation  and  dissemination 
of  bursattee  was  entertained  by  the  natives  of  India  as  early  as 
1820.  Jackson,  in  1842,  seems  to  have  been  the  first  to 
believe  that  there  was  any  connection  between  the  disease  and 
a  fungus. 

Jackson  suggested,  in  1842,  that  the  disease  might  be  re- 
lated to  a  fungus  or  to  a  vegetable  parasite.  Collins,  in  1874, 
expressed  a  similar  belief,  F.  Smith,  in  1879  and  1884, 
seems  to  have  been  the  first  to  have  worked  along  this  line. 
He  was  able  to  find  fungi  in  every  fresh  specimen  of  the 
sores  that  he  examined.  Steel,  in  1 881,  also  found  fungal  ele- 
ments in  these  sores.      T.  Smith,   in    1893,  examined    some 


MORBID    ANATOMY  325 

alcoholic  material  and  gave  expression  to  the  belief  that  the 
disease  was  caused  by  a  fungus.  Fish,  in  1896,  found  a 
fungus  embedded  in  the  diseased  tissue.  He  did  not  name  it 
neither  did  he  obtain  it  in  pure  cul- 
ture, but  his  illustrations  are  ver3' 
clear  in  showing  the  existence  of 
the  fungus.  Fish  gives  in  detail 
the  methods  he  employed.  It  is  to 
his  work  that  we  are  indebted  for 
the  more  careful  description  of  the 
morbid  changes.  Fig.   80.     A  piece  from    the 

lip  of  an  affected  horse,  shozv- 
§  248.  Morbid  anatomy.  As  i"g'  several  diseased  foci 
a  rule  the  lesions  are  near  the  (-^"''^)- 
surface.  Where  the  diseased  portion  has  become  well  de- 
veloped there  is  usually  a  more  or  less  complete  detachment 
of  the  central  inflammatory  growth  from  the  surrounding 
tissue.  This  nodular  or  "kunker"  growth  may  vary  in  its 
density  according  to  the  stage  of  its  development.  During 
the  early  stages  it  is  soft  and  easily  cut ;  later  it  becomes 
firmer  and  ultimately  assumes  a  hard  or  "gritty"  character. 

In  cutting  sections  it  is  generally  the  exception  to  cut 
through  the  nodule  or  kunker  evenly  and  to  have  it  retain  its 
proper  relations  with  the  other  parts.  Even  if  successful  in 
cutting,  the  nodule  drops  out  after  some  of  the  other  processes. 
In  the  specimens  examined  the  lesions  were  confined  entirely 
to  the  skin  and  subcutaneous  tis.sue  ;  no  traces  of  muscular  or 
glandular  structure  were  observed.  Around  the  central  por- 
tion of  the  inflammatory  growth  there  is  a  zone  of  leucocytes 
of  the  mononuclear  and  polynuclear  varieties,  the  latter  pre- 
dominating. They  are  embedded  in  an  abundant  stroma  of 
connective  tissue  which  is  in  a  greater  or  less  stage  of  degen- 
eration. The  central  portion  of  the  zone  is  in  some  cases  very 
closely  packed  with  the  leuococytes,  while  toward  the  peri- 
phery they  are  more  loosely  arranged  and  cause  a  marked 
irregularity  of  the  margin  from  their  uneven  drifting  into  the 
tissue    beyond.     There   is    generally    one    and    perhaps   more 


Fungus. 
Fig.  8i.      J^ai-ions  forms  of  the  fungus. 


MORBID    ANATOMY  327 

points  where  this  infiltration  occurs  quite  extensively.  In 
some  of  the  preparations  the  wandering  cells  have  been  traced 
as  far  as  the  surface  of  the  epidermis. 

Occasionally  there  may   be  found   a  narrow   area  at   the 
periphery  of  the  nodule,  as  seen         /r— v 
in  cross  section,  which  is  lighter       h 
in  color  and  less  dense  in  text- 
ure than  the  central  mass,   evi- 
dently    an     extension     of     the 
growth. 

In  the  specimens  examined 
the  parts  where  the  lesions 
abounded  were  not  character- 
ized by  a  rich  vascular  supply.  Fig  82.  From  the  sa)ne  lip,  but 
The  few  vessels  that  were  en-  sho7ciiig  a  larger  infected  area 
countered  were  not  of  a  normal    V"^^'^)- 

character  ;  their  walls  were  thickened,  and  the  endothelium, 
instead  of  presenting  the  usual  flattened  appearance,  was 
irregularly  cylindrical.  Although  the  condition  was  not  ob- 
served, it  is  not  impossible  that  the  hyphse  of  the  fungus  may 
develop  to  such  an  extent  as  to  compass  or  actually  penetrate 
the  walls  of  the  vessels,  causing  inflammatory  changes  suffici- 
ent to  permit,  in  the  course  of  time,  a  disorganization  or  ab- 
sorption of  a  portion  of  the  vessel  itself,  and  that  ultimately  it 
may  become  incorporated  in  the  nodule. 

DESCRIPTION  OF  FIO.  81. 

1.  Shoiving  a  young  fungus  embedded  in  the  tissues  (/i/>  \. 

2.  Showing  scale-like  bodies  embracing  the  filaments. 

3.  Shoiving  young  branches  of  the  fungus,  and  in  one  place  the 
transparent  sheath.     Hematoxylin  preparation. 

4.  3fycelium  with  scale-like  bodies  lying  among  the  filaments. 
Hematoxylin. 

5.  Vacuolated  filaments.     Hematoxylin. 

6.  Branches  shoiving  a  well  developed,  transparent  sheath.  In 
places  the  axis  of  the  branch  is  disconnected  and  occasionally  there  is 
a  faint  sign  of  a  septum.     Hematoxylin. 

No.  4  ocular,  2  mm.  objective.     Camera  lucida  (.Ifter  Fish). 


328  LEECHES 

The  nodules  are  generally  irregularly  cone  shaped  and  are 
of  variable  size.  In  section  they  reveal  a  very  dense  struc- 
ture, the  framework  of  which  forms  a  close  reticulum. 

Within  the  meshes  are  what  appear  to  be 

jKU^^^  leucocytes  in  various  stages  of  disintegration, 

I   ^^^T     I      and    free   nuclei.     Among    these,    at    places, 

1       there  can   be  seen  small  bodies  of  nearly  the 

Vi&.8:i.y4ntsolai-  same  size  as  the  nuclei  and  taking  the  stains 
■ed  nodtile  show-    •,.  t,i.j-nr--r  a^ 

,,        ,  in   the  same  way,  but  differing  in  form.     At 

tug    the    charac-  .  .       ' ,  ^ 

teristic  rough-  ^^^  portion  of  its  circumference  the  substance 
e  n  e d ,  coral-like  of  the  body  is  seen  to  draw  itself  toward  a 
appearance  of  the  point  and  in  favorable  preparations  that  point 
mass  {Fish).  ^^^  ^^^^^   followed   some  little  distance    as  a 

delicate  filament.  In  most  cases  the  filament  remains  un- 
stained, or,  as  observed  in  a  Gram-eosin  preparation,  the  club 
end  may  stain  blue  and  the  filament  red.  Exceptionally  one 
may  find  a  clear  area  or  vacuole  in  one  of  tlie  clubs.  From 
the  fact  that  the  filament  is  not  usually  traceable  to  its  central 
connection  a  more  or  less  flagellate  appearance  is  given  to  the 
fungus,  which  represents  a  condition  not  believed  to  exist. 

Not  infrequently  small  spherical  bodies  are  found  not  far 
from  the  clubs,  which  take  the  stain  readily  and  whose  size  is 
sufficiently  small  to  admit  of  the  possibility  of  their  being 
spores.  The  free  ends  of  many  of  the  clubs  point  toward  the 
periphery'  of  the  nodule,  but  this  is  not  a  constant  feature. 

The  framework  of  the  nodule  stains  very  slightly  or  not 
at  all  and  shows  among  the  enmeshed  corpuscles  as  a  very 
irregular,  distorted  and  somewhat  glistening  network.  It  is 
this  portion  of  the  nodule  that  gives  the  hard,  gritty  feeling, 
and  is  probably  due  to  a  greater  or  less  deposition  of  lime  salts 
along  the  reticulum.  It  appears  that  the  framework  of  the 
nodule  is  composed  of  a  mycelial  net,  which  in  the  course  of 
development  has  become  more  or  less  calcified. 

As  a  result  of  the  treatment  of  the  nodules  with  a  lo  per 
cent  cold  solution  of  caustic  potash,  a  very  profuse  and  intric- 
ately branched  fungus  became  apparent.  The  branching  is  of 
an  irregular  order.     In   places  there  is  seen  in  the  filament  a 


MORBID    ANATOMY 


329 


central  axis,  which  takes  the  stain,  and  around  this  appears  a 
transparent  or  hyaline  sheath  of  varying  size. 

In  certain  of  the  teased  preparations  (Bioudi-Ehilich 
stain)  the  wall  of  the  filament, 
instead  of  being  smooth  and 
homogeneous,  appears  rough- 
ened, as  if  covered  with  very 
minute  but  numerous  spinous 
processes. 

In  the  sections  of  the  tis- 
sue in  which  the  fungus  ap- 
peared the  substance  of  the 
filament  was  not  uniform.  In 
places  it  was  drawn  together 
in  an  irregular  manner,  with 
intervening  clear  spaces  of 
greater  or  less  area. 

In  some  places  the    fila- 
ments show  distinct  septa,  but 
the    latter    are    not    common. 
Some  of  the  club-like  endings, 
especially  those  that  are  elon- 
gated, show   a  septum   at  the  union  with  the  filament  proper. 
Scattered    among    and    coiled    around    the  ordinary  filaments 
there  have  been  observed  much  more  slender  ones  apparently 
devoid  of  any  external  sheath. 

There  have  also  been  observed  numerous  small  circular 
bodies  of  inconstant  size.  They  have  been  seen  lying  freely 
in  the  meshes  of  the  mycelium  and  also  closely  applied  to  the 
filaments.  These  bodies  are  not  spherical,  but  thin  and  flat- 
tened, and  some  of  them  present  a  curved  appearance,  convex 
on  the  outer  side  and  concave  on  the  inner  side.  They  sug- 
gest the  possibility  of  having  been  closely  applied  to  the  fila- 
ments and  have  something  of  a  scale-like  arrangement.  With 
possibly  one  exception,  no  trace  of  blood  vessels  has  been 
found  in  the  nodules. 


Fig.  84.     The  fungus.      Toluidin 
blue  preparation  ( Fish ) . 


330 


In  the  circumnodular  tissue   pathologic   conditions  exist, 
consisting  of  certain  areas  of  tissue  necrosis. 


Fig.  85.  A  scclio7i  through  a  nodule  shocving  its  deuse  texture,  with 
a  portion  of  its  peripheral  zone  made  up  ofhyphic  'with  leucocytes  inter- 
spersed. Methylene  blue  and  eosin  stain.  No.  4  ocular,  Snun.  objec- 
tive.    Ca  inera  lucid  a  dra  u  •  ing  ( Fish ) . 

There  is  an  infiltration   of  the   connective  tissue   with  a 
great  number  of  wandering  cells.      In   some  places  there  are 


M OR HID    ANATOMY  331 

well-defined  nests  in  the  stroma  of  the  connective  tissue,  simu- 
lating, perhaps,  a  cancerous  appearance.  The  character  of  the 
cells,  which  present  a  curiously  vacuolated  condition,  would, 
however,  tend  to  eliminate  this  view.  The  vacuoles  very  in 
number  and  size,  the  average  number  being  i  to  12  in  a  cell. 

In  some  preparations  numerous  leucocytes,  of  the  mono- 
nuclear and  polynuclear  varieties,  had  drifted  away  from  the 
nodule.  They  were  for  the  most  part  elongated,  and  in  all 
the  nucleus  or  nuclei  appeared  to  be  in  a  healthy  condition. 
The  cells  contained  numerous  eosinophiles,  which  took  a  deep 
orange  color  with  the  Biondi-Ehrlich  stain.  In  places  adjacent 
to  these  leucocytes  there  were  frequently  noticed  a  number  of 
these  small  bodies  apparently  lying  free  in  the  tissue.  No 
definite  cell  wall  was  distinguished  in  the  leucocytes. 

The  vacuolated  cells  are  present  in  greater  numbers  than 
the  heavily  laden  leucocytes.  In  the  former  nuclei  were  pre- 
sent and  presented  various  phases  of  change.  In  some  there 
is  a  single  nucleus,  which  may  be  circular,  crescentic,  or  in 
the  form  of  a  dumb-bell;  in  others  there  may  be  two  or  more 
nuclei  which  in  advanced  cases  appear  only  as  remnants.  In 
extreme  cases  no  nuclei  at  all  are  visible.  The  wall  of  the 
wandering  cell  differs  from  that  of  the  leucocytes  proper  in 
possessing  an  appreciable  thickness.  This  thickened  bound- 
ary apparently  gives  considerable  rigidity  to  the  cells,  as 
nearly  all  of  them  are  approximately  circular  in  form.  Their 
average  diameter  is  about  8  microns.  In  one  specimen  there 
appeared  to  be  large  giant  cells,  measuring  from  1 2  to  18 
microns  and  apparently  possessing  quite  a  distinct  cell  wall. 
Within  each  giant  cell  there  is  some  appearance  of  vacuolated 
cells,  each  with  a  single  nucleus  and  fairly  well-defined  cell 
boundary.  As  many  as  eight  or  ten  of  these  nuclei  have  been 
counted  in  a  single  giant  cell.  There  is  the  possibility  that 
these  apparent  giant  cells  are  simply  some  of  the  vacuolated 
cells  fused  together,  but  the  nuclei  are  well  defined  and  take 
the  stain  very  intensely,  which  is  not  coiniuDiily  the  case  in 
the  ordinary  vacuolated  cells. 

The  connective-tissue  cells  surrounding  the  nodule  show 


332  LEECHES 

marked  signs  of  degeneration,  their  cytoplasm  inmost  cases 
being  extremely  vacuolated.  Among  these  connective-tissue 
cells,  which  for  the  most  part  are  quite  branching  and  elon- 
gated, is  another  class  of  cells  which  are  in  general  of  an  oval 
or  elliptical  form.  The  noteworthy  appearance  of  these  cells 
is  the  presence  of  numerous  dots  in  the  cytoplasm  which  take 
the  methylene  blue  and  toluidin  blue  stains  very  deeply.  The 
appearance  is,  indeed,  very  much  as  if  the  cells  were  filled 
with  micrococci.  These  are  the  granule  cells  of  Waldeyer,  or 
still  further  differentiated  as  the  plasma  cells,  in  contradis- 
tinction to  the  "  mastzellen  "  or  "food  cells,"  which  indicate 
an  exalted  degree  of  nutrition.  The  nucleus  of  the  plasma 
cell  takes  the  stain  very  slightly,  or  not  at  all,  and  is  almost 
entirely  obscured  by  the  numerous  "  granules  "  in  the  cyto- 
plasm. These  cells  are  well  differentiated  by  the  toluidin 
blue  stain,  as  the}'  take  a  deep  purple  color,  while  the  sur- 
rounding cells  are  blue. 

Bitting  has  figured  the  jaw  bone  of  a  horse  quite  exten- 
sively affected  with  this  disease.  He  believes  that  the  lesions 
about  the  mouth  result  from  the  animal  biting  the  affected 
areas  on  the  body. 

Neyrick  reports  finding  the  inflammatory  growths  in  the 
lungs  of  an  affected  subject,  and  Burke  has  reported  them  in 
the  liver.  There  are  no  other  lesions  described  in  the  internal 
organs  although  Neal  writes  that  any  tissue  may  be  invaded. 

§  249.  Treatment.  On  the  ground  that  the  fungus  sup- 
posed to  be  the  cause  of  this  disease  may  be  closely  related  to 
the  ray  fungus  of  actinomycosis,  the  use  of  iodide  of  potas- 
sium has  been  recommended.  It  is  reported  to  be  fairly  suc- 
cessful. The  efficiency  of  this  drug  as  a  specific  needs  further 
confirmation. 

REFERENCES. 

1.  Bitting.  Leeches  or  leeching.  Bullelin  No.  25,  Florida  Agri- 
cultural Experiment  Station,  1894. 

2.  Fish.  A  histological  investigation  of  two  cases  of  an  equine 
mycosis,  with  a  historical  account  of  a  supposed  similar  disease  called 
bursattee  occurring  in  India.      Atinual  Report,  Bureau  of  Animal  In- 


PNEUMONOMYCOSIS  333 

djistry,  U.  S.   Depl.  of  A^ricullure,  1895-6,  p.  229.       (This  report  con- 
tains a  biblioi^raphy  on  Bursaitee. ) 

3.  NiCAi,.  I.eeching  of  horses  and  cattle.  Annual  Report, 
Bureau  of  Animal  Industrv,  U.  S.  Depl.  of  Agriculture,  1887-8.  p. 
489. 


PNEUMONOMYCOSIS. 

^  250.  Species  of  fungi.  The  literature  contains  a  num- 
ber of  reports  of  cases  of  myco.sis  in  the  lower  animals  as  well 
as  in  man  due  to  infection  with  different  moulds.  The  genus 
Aspergillus  seems  to  infect  and  to  produce  lesions  in  animals 
more  frequentl}'  than  the  members  of  other  genera.  In  fact, 
Aspergillus fumigatus^^^\\\%  to  be  the  only  important  pathogenic 
species.  The  lesions  encountered  as  a  result  of  its  invasion  are 
largely  restricted  to  the  respiratory  tract.  Pneumonomycosis 
has  been  reported  in  a  number  of  cases.  Cadeac,  Schneide- 
miihl,  Friedberger  and  Frohuer,  Ostertag  and  Kitt  have  all 
called  attention  to  mycotic  pneumonia.  Renon  considers  the 
lesions  resulting  from  aspergillus  infection  as  a  pseudo-tuber- 
culosis which  he  would  designate  as  "  Aspergillar  tuberculo- 
sis."     Aspergillar  pneumonia  is,  however,  quite  rare. 

^  251.  Description  and  method  of  cultivation  of  the 
mould.  The  aspergillus  fungus  is  readily  cultivated  artifi- 
cially. It  grows  on  most  of  the  ordinary  culture  media  used 
in  bacteriology  if  the  reaction  is  acid  ;  it  develops  poorly  in 
alkaline  media.  The  well-known  Raulin's  fluid  is  reported  to 
be  the  best  medium  for  its  cultivation,  especially  where  the 
aspergillus  must  be  isolated  from  mixed  growths,  as  in  the  ex- 
amination of  sputum.  vSabourand's*  solution  of  maltose  also 
gives  good  results. 


*The  formula  recommended  by  Ravenel  is  as  follows  : 

Maltose,  3  70  grams. 

Peptone,  0.75  grams. 

Distilled  water,  loo.co  c.  c. 
To  this  may  be  addtd  gelatin  or  agar  to  solidify  it,  the  latter  being 

preferable,  as  the  aspergillus  grows  best,  and  forms  fruit  best  at  37°  to 
39°  C. 


334 


PNEUMONOMVCOSIS 


For  ordinary  use  potato,  with  or  without  glycerin,  gives 
excellent  results.  A  paste  made  by  rubbing  up  crumbs  of 
stale  bread  in  water  is  also  a  good  medium.  Growth  is  said 
to  be  more  rapid,  however,  in  Raulin's  fluid  than  in  any  other 
medium,  the  mycelium  appearing  in  from  five  to  twelve  hours 
and  spores  forming  in  from  twelve  to  fifteen  hours.  The 
growth  is  first  a  velvety  white,  soon  becoming  a  delicate  bluish 
green,  which  grows  darker.  On  Raulin's  fluid  it  changes 
after  some  days  to  a  dark  brown.  Cultures  on  potato  retain 
the  green  color  for  a  long  time,  while  those  on  bread  paste 
become  brown. 

The  fungus  retains  its  vitality  in  cultures  for  many 
months  unimpaired.  Its  development  has  been  reported  when 
inoculated  from  cultures  three  or  four  years  old.  Spores  do 
not  form  in  a  temperature  below  20°  C.  and  like  the  mycelium 
they  require  fresh  access  to  oxygen  for  their  best  development. 
They  measure  2.5  to  3//  in  diameter.  In  nature  the  spores  are 
widely  distributed  but  seem  to  be  especially  abundant  in  grain 
and  vegetable  matter.  They  have  considerable  power  of  re- 
sistance to  heat  and  to  chemical 
agents.  They  are  killed  by  a  tem- 
perature of  60°  C.  in  five  and  one- 
half  hours.  In  moist  heat  and  in 
solution  of  bichloride  of  mercury  i 
to  1,000  they  are  destroyed  in 
fifteen  minutes. 

Aspergilhis  fumigatiis  is  dif- 
ferentiated from  other  species  by  its 
color  in  cultures,  the  high  tempera- 
ture at  which  it  grows,  the  size  of 
the  spores  and  by  its  pathogenesis. 
Aspergillus  giaucus  is  the  one  most 
likely  to  be  confounded  with  it.  It 
may  be  differentiated  from  A.  fumi- 
_gatus  by  its  ability  to  grow  at  low  temperature,  its  delicate 
green  color,  the  large  diameter  of  its  spores — 9  to  15/^ — and  its 
lack  of  pathogenic  power. 


Fig.  86.     Aspergillus  fumi- 
gatus  i?!  fruit. 


cri/ri\'ATi()N 


335 


The  mode  of  infection  is  through  the  respiratory  tract. 
Only  a  small  number  of  the  spores  inspired  are  able  to  reach 
the  alveoli,  the  greater  number  of  them  being  arrested  in  the 
tracheal  and  bronchial  secretions.  Hildebrant  has  shown  that, 
having  reached  the  alveoli,  they  penetrate  the  epithelial  lining 
without  difficulty.  Both  animals  and  man  seem  to  possess 
immunity  to  intestinal  infection.  Renon  has  produced  it  only 
a  few  times  experimentalh-. 

The  aspergillus  does  not  form  toxin.  Its  pathogenic 
power  is  due  entirely  to  lesions  produced  by  the  masses  of 
mycelium  which  causes  a  necrosis  of  the  cells  and  a  leucocytic 
reaction  which  diminishes  the  functions  of  the  organs,  the 
final  result  being  an  enfeebled  condition  of  the  animal  and  a 
lessened  resistance  to  hurtful  influences.  When  fruit  hyphae 
can  form,  the  myriads  of  spores  given  off  by  them  may  be 
carried  to  other  parts  of  the  organ.  In  this  way  the  foci 
rapidly  multiply  and  practically  the  entire  organ  becomes 
invaded.  The  opinion  held  by  some  authors  that  in  the  mould 
myco.ses  there  is  "no  fructification  or  actual  multiplication"  of. 
the  infected  agent  and  that  the  "number  of  the  diseased  foci 
corresponds  exactly  with  the  number  of  spores  introduced," 
is  erroneous  both  for  the  disease  naturally  contracted  as  well  as 
for  the  experimental  form.  In  the  produced  lesions,  fruit 
formation  of  the  fungus  is  exceptional.  It  has  been  observed 
by  Renon  to  take  place  only  where  there  is  full  communication 
with  the  air.  It  has  been  observed  only  in  the  lung.  It  is 
extremely  rare  for  aspergillosis  to  pass  from  one  animal  to 
another.     The  infection  can  onl)^  take  place  with  the  spores. 

Piieunionomycosis  in  cattle.  Recently  Pearson  and  Ravenel 
have  described  a  very  interesting  case  of  pneumonomycosis  in 
a  cow  due  to  A.  fiunigatiis.  As  this  seems  to  be  the  only  care- 
fully described  case  in  this  species  of  animals  listed  in  this 
country  their  description  of  the  symptoms  and  lesions  is  very 
largely  incorporated  here.  The  case  was  in  a  Jersey  cow  six 
years  old.  She  had  been  in  poor  condition  for  six  months 
prior  to  bringing  her  to  the  Veterinary  Hospital  where  she  was 
tested  with  tuberculin  with  no  reaction.     At  this  time  she  did 


IE 


,1TY 


336 


PNEUMONOMVCOSIS 


not  eat,  was  weak  and  depressed,  respiration  labored  and  from 
40  to  go  per  minute.  Pulse  rapid.  Percussion  of  the  chest 
walls  gave   a   sound   that   if  anything  was  clearer  and  louder 


Fig.  87.  Composite  drazving  of  section  of  lung  through  nodule  of 
aspergillus  origin.  F,  fibrin  in  alveoli.  S,  fruit  hyphae  and  spores 
of  fungus  (Ravenel). 

than  the  normal  percussion  sound.  Upon  auscultation  it  was 
found  that  the  vesicular  and  bronchial  murmurs  were  consider- 


MORBID    ANATOMY  ^o? 

ably  increased  in  intensity  and  accompanied  here  and  there  by 
sibilant  rales.  She  coughed  violently  at  times.  Six  days 
after  she  came  to  the  hospital  the  breathing  became  more  rapid 
and  difficult  and  the  pulse  very  much  accelerated.  The  animal 
did  not  eat,  grew  weak  rapidly  and  died  four  days  later,  or 
ten  days  after  admission  to  the  hospital. 

§   252.     Morbid   anatomy.       The    anatomical    changes 
given  here  are  restricted  to  the  case  of  Pearson  and  Ravenel. 
The  animal  was  much  emaciated.       The  mucous  membrane  of 
the  small  intestine  was  catarrhal  and  showed  a  small  amount 
of  erosion.       All  the    organs    were   normal  except  the  lungs. 
The   most   striking  feature    on  external  examination  was  the 
extreme  amount  of  emphysema.     The  lobules  were   separated 
from  each  other  by  3  to  5  mm.  and  even  at  some  distance  from 
the  borders  one  could  see  through  the  crevices  by  transmitted 
light.     On  the  surface,  the  sub  pleural   connective  tissue  was 
distended  by  large  blebs.       Upon   palpation  the  lung  crackled 
and  numerous  hard  nodules  could  be  felt.     On  section  numer- 
ous  dark    red    nodules   appeared  in  the   surrounding   normal 
tissue.       In  each  lung  there  were  from  fifty  to  sixty  of  these 
nodules,  from  5  to   12  ram.  in   diameter.       Most  of  them  were 
dark  red  and  closely  resembled  partially  organized  blood  clots. 
However,  on  crushing  a  portion  in  glycerin  between  two  slides 
and  examining  it  under  the  microscope,  they  were  found  to  be 
made  up  almost  entirely  of  a  felted  network  of  mycelial  threads. 
Between    these  large  nodules  there  were   numberless  smaller 
areas  of  much  the  same  color,  i  to  2  mm.  in  diameter,  not  per- 
ceptible to  the  touch  as  nodules  but  which  were  of  the  same 
character  and  were  no  doubt  foci  of  recent  origin.    These  were 
seen  especially  well  in  portions  of  the  lung  which   were  pre- 
served by    Pick's  method,  the    slight  bleaching  of  the  tissue 
bringing  them  into  relief.       On    opening    some   of    the    inter- 
lobular emphysematous   spaces,   small,  whitish,  mouldy  look- 
ing patches  were  noticed  which   bordered  the  cavity.       Scrap- 
ings   of  these    patches  were   made  up  entirely  of  perfect  fruit 
hyphae,  with  myriads  of  spo'-es.       The  diagnosis  of  a  mould 
mycosis  was  in   this  way  made  at   once  and  confirmed  bv  cul- 


338  PNEUMONOMVCOSIS 

tures  and  examination  of  sections.  Cultures  were  made  on 
gl3'cerinated  potato,  bouillon  and  plain  agar,  by  opening  a 
nodule  with  sterile  instruments  and  tearing  out  a  small  portion 
of  the  center,  which  was  transferred  to  the  culture  tubes  and 
placed  in  an  incubator  at  39°  C.  Abundant  growth  was  ob- 
tained on  the  potato  by  the  end  of  thirty-six  hours,  white  at 
first  but  soon  changing  to  a  yellowish  and  later  to  a  dark  green 
color.  The  growth  in  the  bouillon  and  agar  was  slow.  Plates 
and  flasks  of  bread  paste  were  made,  and  these  with  potato 
were  employed  for  all  subsequent  cultures.  The  formation  of 
the  fruit  hyphae  was  studied.  The  spores  measured  from  2.5 
to  3.5//  in  diameter.  By  these  means  the  culture  was  identified 
as  the  aspergillus  fumigatus.  The  experiments  on  other 
animals  were  limited  to  the  inoculation  of  one  rabbit,  into  the 
aural  vein  of  which  one-half  cubic  centimeter  of  a  suspension 
of  the  spores  was  injected.  The  animal  died  in  forty-four 
hours  and  from  the  liver  and  kidneys  cultures  were  recovered. 
All  of  the  organs  were  examined  in  sections,  but  the  mycelium 
was  detected  in  two  only. 

Microscopic  examination.  The  nodules  were  hardened  and 
embedded,  some  in  collodion  and  some  in  paraffin.  Various 
staining  methods  were  tried,  hematoxylin  and  eosin,  carbol- 
thionine.  Gram  and  lithium  carmine  with  Weigert's  fibrin 
stain.  Good  results  were  obtained  with  all,  but  the  carmine 
and  Weigert  gave  the  most  beautiful  picture  and  by  this 
method  the  fungus  was  most  perfectly  demonstrated,  the  spores 
and  mycelium  taking  on  a  deep  purple  color.  The  histology 
was  studied  largely  in  sections  stained  with  hematoxylin  and 
eosin.  The  bronchial  epithelium  was  normal  in  places,  but, 
for  the  most  part,  the  columnar  cells  had  been  replaced  by  a 
sort  of  membrane,  which  appears  to  be  made  up  almost  entirely 
of  a  felt-work  of  mycelial  threads.  From  this  membrane 
hyphae  grew  out  into  the  lumen  of  the  bronchus,  and  here, 
owing  no  doubt  to  the  supply  of  air,  fruit  hyphae  arose,  with 
perfect  sterigmata  and  .spores.  There  was  no  cellular  nor  other 
exudate  and  very  little  debris.  The  under  surface  of  this 
membrane  was  of  looser  texture  and  contained  some   cellular 


MORBID    ANATOMY 


339 


infiltration  made  up  of  round  cells,  leucocytes,  proliferated  con- 
nective tissue  cells  and  red  blood  corpuscles.  The  adjacent 
structures  were  closely  filled  with  a  cellular  infiltration  with  a 
quantity  of  mycelium  of  the  same  description,  this  extended 
to  the  neighboring  alveoli,  which  under  low  power  appeared 
to  have  preserved  their  outline  but  with  greater  amplification 
were  seen  to  have  lost  all  their  normal  structure,  showing 
clumps  of  homogeneous,  irregular  masses  which  stained  faintly 
with  eosin  and  were  probably  of  connective  tissue  origin. 

In  these  areas  the  mycelium  followed  the  alveolar  wall  as 
a  trellis,  the  tissue  seeming  to  afford  no  obstacle  to  its  advance. 
Within  the  alveoli  was  a  finely  granular  debris,  with  some 
coarser  particles,  probably  the  remains  of  cells.  In  sections 
stained  with  carbol-thionine  large  numbers  of  mast  cells  were 
seen  in  the  alveolar  walls.  Bordering  these  degenerated  areas 
were  alveoli  which  had  retained  their  normal  structure  and 
were  filled  with  a  network  of  fibrin  holding  in  its  meshes  a  few 
cells.  In  other  parts  of  the  sections  were  areas  resembling 
those  just  described,  but  in  which  all  anatomical  landmarks 
had  been  destroyed,  so  that  it  was  impossible  to  tell  whether 
or  not  the  spaces  seen  were  bronchi. 

Some  sections  showed  a  widespread  interstitial  and  alveolar 
hemorrhage,  the  blood  showing  a  considerable  increase  in  the 
number  of  leucocytes.  The  capillaries  were  congested  and 
areas  of  edema  with  thickening  of  the  alveolar  walls  were  not 
uncommon. 

There  were  peribronchitis  and  arteritis,  while  in  some  sec- 
tions arterial  thrombosis  was  seen,  the  thrombus  being  pene- 
trated by  mycelium,  though  no  fruit  was  found.  Areas  were 
also  found  in  which  the  alveoli  were  filled  with  a  cellular  exu- 
date producing  consolidation  and  thickening  of  the  alveolar 
walls. 

Emphysema,  both  interstitial  and  vesicular,  were  marked 
and  often  extreme.  Around  the  borders  of  the  interstitial 
cavities  was  a  distinct  zone  made  up  of  red  blood  cells,  leuco- 
cytes and  homogeneous  material,  which  was  yellowish  in  fresh 
as  well  as  stained  sections.     These  areas  contained  very  little 


340 


PNEUMONOMYCOSIS 


mycelium.  All  sections  showed  a  small  amount  of  anthracosis. 
The  appearance  of  sections  varied  in  different  nodules  as  they 
were  taken  further  and  further  away  from  the  center.  In 
general  the  fungus  was  thickest  at  the  center,  so  thick  in 
many  instances  that  the  lung  tissue  was  hidden  entirely, 
and  grew  less  as  we  went  outward.  The  tissue  changes  noted 
took  place  in  a  zone  beyond  the  greatest  growth  of  the  fungus. 
In  other  nodules  the  fungus  was  evenly  distributed  throughout, 
following  the  alveolar  walls.  In  these  the  tissue  changes  were 
slight.  At  times  the  fungus  grew  in  dense,  brush- like  clusters, 
closely    resembling     actinomycosis    under   low    amplification. 

This    form    was 
""  considered    to    show 

a  marked  reaction 
and  resistance  on  the 
part  of  the  animal 
and  a  lowered  vital- 

L'  im'^'V  "<     'S^^m^ssmyst       ^^^  ^°  ^^^  fungus. 

r^8?^'*C^r     >_j^^^^^^^S  When  found  it  indi- 

fV^M^'     '         '^"'^"^^^^^^G^  -        cated  that  the  asper- 

mvHj'^ '  ^^^^^«^n      gliosis    was    a    pri- 

i^^)k*hl^  y^  ^^^^^§a  rnary  and  not  a  sec- 

itt;«.-li«.  -^tl  :^2i^^^      ondary    or    terminal 

affection.  No  giant 
cells  were  found  in 
any  section. 

Fruit  formation 
was  not  observed  in 
the  substance  of  the 
tissues  at  any  time. 
It  was  observed  most 
frequently  in  bronchi,  which  were  for  the  most  part  denuded 
of  their  epithelium,  and  next  in  emphysematous  cavities, 
where  it  could  be  detected  in  clusters  by  the  naked  eye.  Fruit 
was  found  in  sections,  in  spaces  the  nature  of  which  it  was 
impossible  to  determine  accurately.  Whenever  the  formation 
of  fruit  was  seen,  there  were  innumerable  free   spores  as  well 


Fig  88.  Necrosis  in  the  kidney  of  a  rabbit 
due  to  A.  funiigatus  ;  A.,  fmigus  ;  B  and  C, 
nuclei;  D,  tiecrotic  tissue  ;  E,  normal  cells. 


MORRID    AXATOMV  341 

as  those  still  attached  to  the  sterigmata,  but  in  no  case  were 
spores  detected  in  the  substance  of  the  tissues. 

In  many  sections,  especially  those  from  near  the  center  of 
the  nodules,  the  mass  of  mycelium  was  so  dense  that  the  struc- 
ture of  the  tissues  was  obscured.  Besides  the  dense  growths 
resembling  actinomycosis  already  described,  other  brush-like 
clusters  not  unlike  them  were  frequently  seen.  These  differ 
from  the  former  in  being  somewhat  less  compact,  and  that 
from  their  periphery  numerous  hyphae  run  out  into  the  sur- 
rounding tissues,  whereas  in  the  actinomycotic  form  the  masses 
are  sharply  defined  and  only  here  and  there  a  few  threads 
grow  out  beyond  the  cluster.  Their  appearance  suggests  that 
they  mav  be  actinomycotic  forms  which  have  finally  overcome 
the  resistance  of  the  tissues.  Emphysema  is  less  marked  in 
the  neighborhood  of  the  latter. 

The  cow  was  examined  carefully  for  the  lesions  of  tuber- 
culosis and  in  one  lung  some  four  or  five  caseous  and  calcare- 
ous nodules  i  cm.  in  diameter  were  found,  in  which  tubercle 
bacteria  were  demonstrated,  but  no  mycelium  could  be  de- 
tected. In  no  part  of  the  lung  was  there  coexistence  of  the 
two  infections. 

The  fact  that  the  animal  did  not  react  to  tuberculin, 
although  tuberculosis  was  present,  is  noteworthy  and  suggests 
that  the  mould  infection  may  interfere  with  the  test.  It  is 
probable  that  the  tuberculous  lesion  was  arrested  in  its 
progress. 

§  253.  Pulmonary  mycosis  in  birds.  Mohler  and 
Buckley  have  recently  described  a  case  of  this  affection  in  the 
lung  of  a  flamingo  which  died  at  the  National  Zoological  Park 
in  Washington.  In  this  case  the  bird  was  very  much  ema- 
ciated. The  lungs  presented  lesions  suggesting  those  of  tu- 
berculosis in  their  general  appearance.  The  other  organs 
(liver,  spleen  and  kidneys)  appeared  to  be  normal.  From  the 
lung  Aspergillus  fumigatus  was  obtained.  [The  authors  give 
a  full  description  of  the  lesions  with  a  historical  sketch  and 
results  of  experiments  on  the  smaller  animals.] 


342  EPIZOOTIC    LYMPHANGITIS 

REFERENCES. 

1.  Arwine  and  Lamb.  A  fifth  case  of  "  fungous  foot  "  in  America. 
The  Anier.  Jour.of  Med.  Sciences,  Oct.  1899. 

2.  DiNWiDDiE.  On  the  toxic  properties  of  moulds.  Biilletiti  No. 
JO,  Arkansas  A o-ric.  Exp.  Sta.,  May,  1896. 

3.  Flexner.  Pseudo-tuberculosis  Hominis  Streptothricha.  The 
Jotcrnal  of  Experimental  Medicine,  Vol.  Ill  (1898).   (Bibliography). 

4.  MoHLER  AND  Buckley.  Pulmonary  mycosis  in  birds— with  a 
report  of  a  case  in  a  flamingo.  Annual  Report  of  the  Bureau  of  Animal 
Industry,  igoj.     {Also  issued  as  circular  No.  j8. ) 

5.  Ophuls  and  Moffitt.  A  new  pathogenic  mould.  The  Phila- 
delphia Med.  fournal,  June  30,  1900. 

6.  Pearson  and  Ravenel.  A  case  of  pneumonomycosis  due  to 
the  Aspergillus  fumigatus.  The  (Jtiiversity  Medical  Magazine,  Aug. 
1900.      The  Vet.  Journal,  New  Series,  Vol.  II  (1900),  p.  229. 

7.  Rknon.  L'etude  sur  I'aspergillose  chez  les  animaux  et  chez 
I'homme.     1897. 

8.  Weis.  Four  pathogenic  Toruhe  (Blastomycetes).  The  Jour. 
of  Med.  Research,  Vol.  VII  (1902),  p.  280. 


EPIZOOTIC   LYMPHANGITIS 

Symonyms.  Japanese  farcy  ;  pseudo-farcy  ;  equine  pox  ; 
equine  syphilis  ;  inundation  fever. 

§  254.  Characterization.  Epizootic  lymphangitis  is 
described  as  a  virulent  infectious  disease  characterized  by 
suppuration  of  the  superficial  lymphatic  vessels,  due  to  the 
presence  of  a  specific  organism.  It  is  a  disease  of  the  solipeds, 
although  Tokishige  reports  finding  it  in  cattle  in  Japan. 

§  255.  History.  This  affection  seems  to  have  been 
known  for  a  very  long  time  and  to  have  been  confused  with 
cutaneous  glanders  (farcy).  French  veterinarians  have  recog- 
nized the  disease  as  river  ic^rcy ,  farcin  en  ciil  de  poule,  curable 
or  benign  farcy.  In  France  these  various  forms  were 
acknowledged  to  be  identical,  the  "river  farcy  "  being  consid- 
ered as  an  attenuated  form  of  glanders  (farcy)  until  1873, 
when  Rivolta  discovered  the  specific  organism  {^Saccharomycosis 


ETIOLOGY 


343 


farciminosus).  This  affection  has  been  recognized  at  different 
times  in  Japan,  China  and  India.  It  has  been  known  in 
Algiers  for  many  years  and  during  the  war  in  South  Africa  it 
seems  to  have  been  introduced  there.  From  South  Africa  it 
has  been  imported  into  England  and  Ireland  by  government 
horses  returning  from  the  Cape.  The  first  case  in  England 
appears  to  have  been  detected  in  1902.  In  1907,  Pearson  dis- 
covered it  in  western  Pennsylvania. 

§  256.  Etiology.  This  disease  is  caused  by  an  organism 
described  by  Rivolta  as  Saccharomyces  farmninosns.  It  is  also 
called  a  cryptococcus.  According  to  Pallin,  it  is  found  in 
large  numbers  in  the  diseased  tissues  and  products,  partly 
free  and  partly  enclosed  in  pus  corpuscles,  which  often  con- 
tain from  ten  to  thirty  or  more  of  them.  It  is  characterized 
by  its  clearly  defined  contour  and  its  very  refractile  double 
outline.  It  measures  from  3  to  4  //  in  diameter,  and  in  the 
unstained  preparations  it  is  said  to  be  best  seen  with  an  oil 
immersion  and  abbe  condenser,  under  a  magnification  of  not 
le.ss  than  800  diameters.  In  stained  preparations  it  can  be 
recognized  with  a  much  lower  magnification. 

The  classification  of  this  organism  has  been  much  dis- 
cussed by  several  workers.  Canalis  places  it  with  the  coccidia, 
Piana  and  Galli-Valerio  consider  it  as  belonging  to  the  proto- 
zoa, and  Formi  and  Aruch  as  a  blastomycete.  Tokishige 
and  Marconi  believe  that  it  belongs  with  the  saccharomyces. 
It  is  not  easily  stained  by  the  aniline  dyes,  although  Mettam 
has  shown  that  by  the  Gram  method,  Nicolle's  violet,  Nicolle's 
thionine  and  others  it  is  readily  colored.  It  is  cultivated  with 
difficulty.  Tokishige  obtained  cultures  in  bouillon,  agar, 
gelatin  and  on  potato.  In  bouillon  it  required  seventeen  days 
to  obtain  a  growth. 

The  infectious  material  may  be  transported  by  contact 
between  the  diseased  and  well  horses,  by  stall  bedding,  by 
stable  utensils  and  harnesses  and  possibly  by  insects. 

The  period  of  inciibatio7i  \'s>  placed  at  from  three  weeks  to 
three  months  and  in  certain  cases  it  may  extend  to  even  eight 


344  EPIZOOTIC    LYMPHANGITIS 

or    ten    months.       In    experimental    cases    symptoms    have 
appeared  after  32  days. 

§257.  Symptoms.  An  infection  takes  place  in  wounds, 
the  first  symptom  usually  appearing  at  the  seat  of  a  pre-exist- 
ing wound.  The  lesions  usually  appear  in  the  skin,  but  they 
may  occur  on  a  mucous  membrane.  They  consist  of  swelling 
and  suppuration  of  the  lymph  vessels  and  glands.  These 
break  and  discharge  a  thick,  yellow  pus,  stained  with  blood. 
Pearson  states  that  the  horses  do  not,  as  a  rule,  show  any 
general  disturbance  except  in  very  advanced  cases.  Pallin 
describes  the  opened  sores  as  follows  : 

"  The  buds,  ulcers,  or  sores,  by  all  of  which  names  they 
are  known,  are  characterized  by  their  bright  red  exuberant 
granulations  and  their  fungoid  appearance,  as  well  as  by  their 
indurated  base  and  well-defined  edges  ;  the  adjoining  skin, 
which  is  partially  inverted,  has  a  peculiar  shiny  appearance  ; 
an  opening  exists  in  the  center  of  the  bud,  from  which  the  pus, 
at  first  creamy,  and  afterwards  yellov^ish,  oily,  and  curdled,  is 
continually  discharging."' 

These  buds  are  quite  different  from  those  of  glanders. 
The  lesions  are  commonest  in  the  limbs.  The  most  usual 
location  is  on  the  fore-leg  generally  extending  up  along  the 
fore- arm  to  the  brachial  region  and  point  of  the  shoulder. 

The  sores  vary  in  size  from  that  of  a  pea  to  a  hen's  egg. 
Pallin  reports  lesions  on  the  mucous  membranes  in  from  7  to 
10  per  cent  of  the  cases.  When  these  occur  on  the  nasal 
mucosae  they  are  liable  to  be  confounded  with  those  of 
glanders. 

Usually  the  general  symptoms  are  not  conspicuous.  The 
temperature  remains  normal  and  the  appetite  good.  The 
disease  seems  to  thrive  best  on  animals  in  good  condition. 

Pearson  describes  its  symptoms  as  follows:  "The  most 
common  manifestation  consists  in  the  presence  of  small, 
chronic,  discharging  ulcers  in  the  vicinity  of  the  hock 
joint  of  a  thickened  hind  leg.  In  such  a  case,  one  may  also 
find  small  scars  showing  where  ulcers  have  healed   and   there 


MORBID    ANATO:\IV 


345 


will  probably  be  some  firm  nodules  beneath  the  skin  and,  per- 
haps, one  or  more  nodules  that  have  softened,  forming  fluctu- 
ating abscesses.  The  regional  lymphatic  ducts  are  corded  and 
the  glands  inside  the  thigh  are  hardened  and  nodulated. 

"  The  earliest  observed  symptom  may  be  the  occurrence  of 
a  firm  nodule,  from  the  size  of  a  pea  to  that  of  a  walnut, 
beneath  the  skin,  anywhere  on  the  body.  Corded  lymphatics 
extend  from  this  lesion.  In  time,  the  nodule  will  soften  and, 
at  length,  its  purulent  contents  will  break  through  the  skin. 
The  time  required  for  these  developments  is  most  variable  and 
may  reach  several  weeks.  Such  pus  is  thick  yellowish  or 
greyish  yellow  and  often  it  is  mixed  with  blood.  Sometimes 
it  contains  flakes. 

"  In  other  cases,  the  first  symptom  observed  is  an  indolent 
sore,  covered  with  pus  and  scab,  surrounded  by  a  slightly 
swollen  zone  and  from  which  one  or  more  firm  cords  extend 
beneath  the  skin  toward  the  lymphatic  glands.  This  condition 
is,  no  doubt,  the  first  to  develop,  but  such  a  sore  often  escapes 
special  notice  until  nodules  occur. 

' '  Fresh  ulcers  may  be  surrounded  by  a  slightly  rai.sed 
zone  of  bright  red  granulation  tissues  ('proud  flesh').  The 
ulcers  occur  irregularly  and  they  disappear  slowly  ;  some  heal 
in  a  fortnight,  others  continue  to  discharge  for  months,  and, 
after  healing,  may  break  out  again.  From  this  long  continued 
irritation  and  from  the  formation  of  scar  tissue,  the  skin  thick- 
ens and  the  affected  parts  become  indurated. 

"  Ulceration  sometimes  occurs  upon  the  conjunctiva  and 
on  the  mucous  membrane  of  the  nostrils  and  upper  respiratory 
act .'" 

§  258.  Morbid  Anatomy.  This  disease  consists  in  an 
inflammation  of  the  lymphatics.  On  .section  the  walls  of  the 
vessels  are  thickened,  their  internal  membrane  is  congested, 
and  the  ducts  filled  with  thick-clotted  lymph  mixed  with  pus, 
which  is  followed  by  the  formation  of  the  abscesses  (pustules) 
and  granulating  .sores.  The  affected  parts  become  indurated 
as    the    result    of    the    formation  of  fibrous  tissue  due  to  the 


346  MISCELLANEOUS    FUNGOUS    INFECTIONS 

inflammation  set  up  by  the  disease.  On  the  mucosa,  the 
ulcers  have  a  round,  well  defined  raised  border.  They  are  at 
first  isolated  but  later  they  become  confluent.  Nodules  are 
occasionally  found  in  the  liver  and  spleen.  A  few  horses 
appear  to  recover  spontaneously.  A  few  are  apparently  bene- 
fitted by  proper  treatment.  It  is  said  to  be  fatal  in  from  lo  to 
15  per  cent  of  all  cases. 

§  259.  Differential  diagnosis.  This  affectibn  is  to  be 
differentiated  from  glanders,  ulcerative  lymphangitis,  tuber- 
cular lymphangitis,  bursatti,  and  the  so-called  botryomycosis. 
The  finding  of  the  specific  organism  in  case  of  epizootic  lym- 
phangitis affords  a  positive  means  for  its  difi'erentiation  and 
diagnosis. 

REFERENCES. 

1.  MetTam.  The  staining  of  the  organism  of  epizootic  lymphan- 
gitis.    The  Vet.  Record,  Vol.  XVI  (1904),  P-  834. 

2.  Pallin.     a  treatise  on  epizootic  lymphangitis.     London,   1904. 
5.     Pearson.   Epizootic  lymphangitis  of  horses  and  mules.     Cir- 
cular No.  S,  Pennsylvania  State  Livestock  Sanitary  Board  (1907). 


MISCELLANEOUS   FUNGOUS   INFECTIONS. 

^  260.  Farcy  in  cattle.  This  affection  is  described  as 
being  characterized  by  an  inflammation  tending  to  suppura- 
tion of  the  superficial  lymphatic  vessels  and  glands  caused  by 
a  streptothrix.  The  descriptions  of  this  affection,  however, 
are  not  recent,  those  by  Cruzel,  1869,  and  Nocard  in  1888 
being  among  the  latest,  and  consequently  there  is  some  ques- 
tion concerning  its  etiology.  Nocard  states  that  it  is  very 
closely  related  to  actinomycosis. 

This  affection  is  said  to  be  chronic,  attacking  the  lymph 
vessels  and  glands,  which  become  hard  and  often  caseous. 
Tokiskye  has  described  cases  in  which  the  lesions  extend  into 
the  respiratory  passages.  In  some  cases  abscesses  occur. 
They  are  reported  to  occur  on  the  ventral  surface  of  the  bod}'. 


MYCOTIC    STOMATITIS  347 

This  disease  does  not  appear  to  exist  in  this  country. 
Until  its  differentiation  from  tuberculosis,  actinomycosis  and 
"  botryomycosis"  is  made  its  real  nature  will  remain  in  doubt. 

1.  Cru/.ki-.     Traite  des  maladies  de  I'espcce  bovine.     i.SSg. 

2.  Mausis.     M6moire  sur  le  farcin.     Ibid. 

3.  NoCARD.  Note  sur  la  maladie  des  boeufs  connue  a  la  Guade- 
loupe sous  le  nom  de  farcin.    Aiiiiales  de  V lust.  Pasteur,  Vol.   II  (18S8), 

p.  293- 

4.  SoRiLLOX.  Exemples  de  farcin  dans  le  boeuf.  Recueil  de  yned. 
vHer.,  1829,  p.  651. 

§  261.  Mycotic  stomatitis  in  cattle.  Cattle  some- 
times suffer  from  stomatitis  caused  by  fungi.  The  exact 
species  that  are  involved  in  this  form  of  infection  are  not 
clearly  determined.  A  number  have  been  incriminated. 
Mohler  has  recently  described  a  stomatitis  of  this  character. 
The  symptoms  are  inability  to  eat,  suspension  of  rumination, 
frequent  movements  of  the  lips,  and  in  some  cases  dribbling  of 
saliva.  There  is  a  desire  to  eat  but  prehension  is  difficult. 
The  mouth  is  abnormally  warm  and  the  mucosa  reddened, 
rarely  small  blisters  will  be  seen  which  soon  develop  into 
ulcers.  These  vary  in  diameter  from  3  to  25  mm.  The 
erosions,  which  may  become  confluent,  are  found  on  the  gums, 
dental  pad,  inside  of  the  lips  and  on  the  end  of  the  tongue. 
They  also  occur  on  the  cheeks.  The  ulcers  are  hemorrhagic 
at  the  borders.  The  central  necrotic  portion  soon  sloughs, 
and  the  place  is  filled  with  granulating  tissue.  There  are 
often  erosions  and  exfoliation  of  the  epithelium  of  the  muzzle. 
There  are  at  times  swellings  about  the  feet. 

The  prognosis  is  good. 

The  course  of  the  disease  varies  from  7  to  15  days,  the 
average  being,  according  to  Mohler,  about  10  days.  Ward 
has  diagnosed  a  mycotic  stomatitis  in  California.  This  infec- 
tion, which  appears  to  occur  in  enzootics,  resulting  from  the 
eating  of  food  containing  irritant  fungi,  is  to  be  differentiated 
from  foot-and-mouth  disease,  ergotism,  and  necrotic  stomatitis 
caused  bv  B.  necrosis. 


348  MISCELLANEOUS    FUNGOUS    INFECTIONS 

MoHLER.  Mycotic  stomatitis  of  cattle.  Circular  No.  51.  Bureau 
of  Atiimal  Industry,  U.  S.  Dept.  of  Agric.     1904. 

§  262.  Blastomycetes  infection  in  horses.  Fermi 
and  Aruch  described  a  disease  in  horses  resembling  glanders 
except  that  it  did  not  affect  the  lungs,  which  was  caused  by  a 
blastomycete.  It  is  known  as  Farcin  d' Afriqiie.  Central- 
blattf.  Bak.,  Bd.  XVII  (1895),  p.  593. 

Frothingham  has  described  a  tumor-like  lesion  in  the 
lungs  of  horses  caused  by  a  blastomycete.  The  growth  was 
about  ten  inches  in  diameter  and  on  section  resembled  in 
appearance  a  myxosarcoma.  The  central  portion  was  easily 
removed,  the  outer  zone  forming  a  firm  border  wall  composed 
of  fibrous  tissue.  A  microscopic  examination  of  the  central 
portion  showed  it  to  consist  of  a  fine  meshwork  of  fibrous 
tissue,  in  the  meshes  of  which  were  many  cells  and  blasto- 
myces.  These  were  fatal  to  rabbits  and  guinea  pigs.  Jour. 
Compar.  Med.  and  fW.   Archives,  Vol.  XXIII  (1902),  p.  593. 


CHAPTER    IX 

DISEASES    CAUSED    BY   PROTOZOA 
GENUS    PIROPLASMA. 


§  263.  General  discussion  of  piroplasma.  There  are 
several  species  of  piroplasma.  Their  life  history  is  not  known. 
In  the  infected  animal  they  live  within  the  blood,  often  enter- 
ing into  and  destroying  the  red  blood  corpuscles.  They  are 
transmitted  from  the  infected  to  the  uninfected  animal  by 
means  of  some  insect  usually  a  tick.  The  known  species  of 
this  genus  are  parasitic  and  pathogenic  in  different  species  of 
animals.  The  term  Piroplasmoses  was  introduced  by  Nocard 
to  designate  the  diseases  produced  by  these  organisms.  Ac- 
cording to  his  classification  Piroplasmoses  are  diseases  resulting 
from  infection  wuth  any  species  belonging  to  the  genus 
Piroplasma.  Nocard  recognizes  four  species,  but  others  have 
been  described  more  recently. 

Piroplasma  bigemifium—iho.  piroplasma  of  cattle. 

Piroplasma  ^^z.s— the  piroplasma  of  sheep. 

Piroplasma  canis — the  piroplasma  of  dogs. 

Piroplasma  equi — the  piroplasma  of  horses. 

To  Americans,  Piroplasma  bigemiyium,  the  form  infecting 
cattle,  is  the  most  important. 


TEXAS    FEVER. 

Synonyms.  Bovine  malaria;  red  water;  Spanish  fever; 
splenic  iever;  "  bloody  murrain;"  southern  cattle  fever;  tick 
fever. 


350  TEXAS    FEVER 

i^  264.  Characterization.  Texas  fever  is  an  infectious 
blood  disease  of  cattle,  characterized  by  rise  of  temperature, 
hemoglobinuria,  destruction  of  the  red  blood  corpuscles  and 
the  presence  in  the  blood  of  a  protozoan  parasite  which  is 
transmitted  from  animal  to  animal  by  means  of  the  cattle  tick. 

It  is  believed  to  be  identical  with  the  hemoglobinuria  in 
Roumania,  tick  fever  in  Australia,  and  "La  Tristeza "  in 
South  America.  It  has  been  named  inalaria  des  bovides  by 
Celli  and  Sentori  and  Malaria  bovine  by  Lignieres.  Although 
it  dififers  in  many  ways  from  human  malaria,  the  analogy  is  so 
close  respecting  the  specific  cause,  wide  distribution  and  means 
of  transmission,  that  bovine  malaria  seems  to  be  a  very  suit- 
able name  for  this  affection.  At  least  it  has  the  advantage  of 
not  stigmatizing  any  locality. 

The  peculiar  and  interesting  feature  of  this  affection  is 
the  fact  that  cattle  raised  in  the  infected  districts  become  im- 
munized so  that  they  do  not  suffer  from  the  disease  but  they 
carry  its  specific  organism  in  their  blood.  When  imported 
into  non-infected  districts,  they  transmit  the  virus,  by  means 
of  the  cattle  tick,  to  susceptible  animals,  but  remain  them- 
selves perfectly  well. 

§  265.  History,  There  is  little  knowledge  concerning 
the  early  history  of  this  disease.  With  the  development  of 
commerce,  however,  the  shipping  and  interchange  of  animals 
gradually  came  into  prominence  and,  with  it  all,  this  disease 
which  had  long  been  known  in  certain  localities  was  more 
widely  scattered  until  finally  it  came  to  be  an  important  barrier 
to  the  cattle  traffic.  In  1868,  this  disease  seems  to  have  made 
its  first  important  impression  upon  the  American  people.  In 
June  of  that  year,  Texas  cattle  were  shipped  up  the  Mississippi 
river  to  Cairo  and  thence  by  rail  into  the  states  of  Illinois  and 
Indiana,  where  they  caused  during  the  summer  enormous 
losses  from  this  disease.  Cattle  from  these  states  shipped  east 
brought  the  disease  with  them.  The  cattle  commissioners  of 
New  York  and  the  Board  of  Health  of  New  York  City  endeav- 
ored to  check  the  importation  of  such  cattle.     The  disease  was 


GEOGRAPHICAL    DISTRIBUTION  351 

careful!}'  investigated  at  that  time  but  nothing  beyond  a  very 
accurate  description  of  the  gross  lesions  was  obtained.  Later, 
Salmon  determined  the  boundary  line  between  the  non-infected 
and  the  permanently  infected  districts,  or  what  is  now  known 
as  the  Texas  fever  line.  (See  Plate  II).  In  1889,  the  Bureau 
of  Animal  Industry  undertook  a  systematic  investigation  into 
the  nature  of  this  disease,  which  resulted  in  the  same  year  in 
the  discover}^  of  its  specific  cause  by  Dr.  Theobald  Smith  and 
later  the  demonstration  of  the  fact  that  the  disease  is  trans- 
mitted from  southern  to  northern  cattle  through  the  medium 
of  the  cattle  tick.  Prior  to  this  (1888),  v.  Babes  had  found 
an  intraglobular  parasite  in  the  blood  of  cattle  suffering  from 
an  epizootic  disease  (hemoglobinuria )  in  Roumania.  While 
at  first  these  diseases  were  thought  to  be  diflferent  in  their 
etiology  they  are  now  believed  to  be  identical. 

A  number  of  investigations  have  been  made  by  the  Bureau 
of  Animal  Industry,  the  State  Experiment  Station  and  State 
Board  of  Agriculture  of  Missouri  and  Texas,  the  Louisiana 
Experiment  Station  and  by  the  Queensland  Government, 
Australia,  for  the  purpose  of  obtaining  a  practical  method  for 
the  production  of  immunity  against  Texas  fever  in  susceptible 
cattle.  The  results  that  are  being  obtained  are  promising,  as 
they  have  made  it  possible  to  take  northern  cattle  into  the 
infected  territory  of  the  south. 

j^  266.  Geographical  distribution.  In  the  United  States 
the  distribution  of  Texas  Fever  corresponds  with  that  of  the 
cattle  tick  {Boophihis  annidatus) .  This  includes,  with  pos- 
sibly a  few  small  exceptional  areas,  that  portion  of  the  country 
south  of  the  "Texas  fever  line"  which  is  shown  by  a  red  line 
on  the  accompanying  map  but  which  is  changing  constantly 
by  virtue  of  the  spread  or  elimination  of  the  tick.  It  has  been 
identified  with  the  tick  fever  of  Australia  which  has  become 
a  source  of  great  loss  to  the  cattle  industry  of  that  country. 
Lignieres  has  identified  the  disease  in  South  America  (Argen- 
tine Republic).  It  is  also  reported  to  be  identical  with  a 
malady  affecting  cattle  along  the  Danube  river,  in  the  Balkan 


352  TEXAS    FEVER 

provinces  and  in  South  Africa  (Rhodesia  Rotwasser*).  It  is 
restricted,  however,  to  those  countries  where  the  climate  is  not 
sufficiently  severe  to  destroy  the  cattle  tick  during  the  winter 
season  and  where  the  animals  are  constantly  infected.  Cattle 
(genus  Bos)  are  the  only  animals  which  suffer  from  it. 

§  267.  Etiology.  Texas  fever  is  caused  by  a  microor- 
ganism belonging  to  the  protozoa  and  named  by  Smith,  the 
discoverer,  Pyrosoma  bigeniinum.-\     It  is  generally  recognized 


*The  Rhodesian  redwater  or  East  African  coast  fever  is  according  to 
Stockman's  report  a  very  different  disease  from  the  tick  fever  in 
America.     The  conclusions  from  Stockman's  report  are  as  follows  : 

1.  That  the  disease  is  caused  by  a  special  blood  parasite — a  piro- 
plasma. 

2.  That  it  is  a  disease  peculiar  to  bovine  animals. 

3.  That  it  is  only  indirectly  contagious  ;  that  is  to  say,  a  sick 
animal  will  not  infect  another  susceptible  animal  by  contact,  however 
intimate,  or  by  any  of  the  excretions  or  fluids  of  its  body,  as  in  the  case 
of  rinderpest  and  like  diseases. 

4.  That  the  indirect  agents  of  infections  are  the  nymphal  and  adult 
stages  of  the  brown  tick  (Rhisicephalus  Appendiculatus)  and  the  black 
tick  (R.  Simus?).     The  former  however  is  the  more  important  factor. 

5.  That  only  those  ticks  which  in  one  of  their  intermediate  stages 
have  sucked  on  affected  animals  are  capable  of  transmitting  the  disease 
to  other  oxen. 

6.  That  the  infecting  agent  does  not  pass  through  the  egg  of  the 
tick  to  the  second  generation,  as  was  at  first  thought  probable,  by 
reasoning  from  analogy  with  what  takes  place  in  the  blue  tick  in  case  of 
Texas  fever. 

7.  That  the  brown  and  black  ticks  existed  in  certain  parts  of  the 
Transvaal  long  before  the  disease  was  imported  and  that  the  said  ticks 
only  become  virulent  after  sucking  sick  animals  recently  introduced. 
These  species  of  ticks  exist  to-day  on  many  farms  that  are  perfectly 
clean,  and  which  will  remain  clean  as  long  as  sick  animals  are  kept  off 
them. 

8.  That  the  blue  tick  is  not  a  carrier  of  the  disease. 

9.  That  the  proportion  of  recoveries  from  the  disease  is  five  per 
cent,  at  the  very  most. 

tThe  genus  of  the  parasite  has  been  changed  to  Piroplasma  by  Pat- 
ton,  to  Apiosomahj  Wandelleck,  to  Accnibosporidies  by  Bouome,  and 
Porteus  virnlentissimus  by  Perroncito.  vStarcovici  has  named  the  organ- 
ism described  by  Babes  as  Hematococcus,  Babesia  bigeminum  bovis. 


\\  U  ^\A 


-'-H^ 


ETIOLOGY 


353 


that  Piroplasma  is  the  proper  generic  term  and  this  is  used  by 
writers  on  protozoa. 

If  Texas  fever  in  America   and   hemoglobinuria  in    Rou- 
mania  are  ident- 
ical,   Babes  was  

the   first   to  call      \^  ^^  )  \q   )  ^^) 

attention   to  the 

existence  of  this        ^^^^-  ^9-     P^'opiasma  bt^euunnm  in  red  blood 

corpHsdes. 
mtraglobular 

parasite.  It  seems  that  Dr.  Stiles,  in  1867,  observed  this  or- 
ganism but  failed  to  recognize  its  significance.  It  is  found  in 
the  blood  in  cases  of  Texas  fever  and  it  also  exists  in  the 
blood  of  immune  animals  in  the  tick  infested  districts.  The 
life  history  of  this  parasite  is  not  determined.  In  the  blood 
of  the  diseased  animals  they  appear  in  the  unstained,  fresh 
preparation,  as  minute  or  larger  bright  bodies  which  may  be 
from  0.5  to  4.o/<  in  diameter  according  to  the  form  of  the 
disease.  In  the  acute  types  of  the  disease  certain  of  the  red 
corpuscles  contain  pale  or  brighter  pyriform  shaped  bodies. 
One  end  of  each  body  is  broad  and  rounded,  the  other  tapering 
and  pointed.  Usually  there  are  two  of 
these  bodies,  both  of  the  same  size,  in  a 
corpuscle.  More  rarely  there  is  but  one, 
although  four  are  occasionally  observed 
(Fig.  91).  When  two  are  present  the 
tapering  ends  approach  each  other  and 
usually  they  are  joined  while  the  other 
ends  may  point  in  any  direction.     Several 

forms    have    been    noted    varying    from    a    ^  ^ 

•  1  ,         ,.  ^,  ,,     Fig.    90.     Coccus 

round  to  a  pyramidal  outline.  The  small  y^rw^  of  Piroplas- 
and  often  the  larger  bodies  have  been  ma  bigeminum. 
observed  to  change  their  position  within 
the  red  corpuscle.  Smith  has  noted  that  the  ameboid  bodies 
observed  were  apparently  single  within  the  corpuscle.  In 
dried  and  heated  cover- glass  preparations  stained  with  alka- 
line methylene  blue,  these  parasites  are  distinctly  colored. 
They   are  also  stained   with   carbol   fuchsin  and   with   heme- 


354 


TEXAS    FEVER 


Fig.  91.  Blood  from 
kidney  shoicing  para- 
sites of  Texas  fever 
(Smith). 


toxylin.  As  a  rule  they  stain  more  deeply  in  preparations 
made  from  internal  organs  than  they  do  in  those  from  the 
living  blood. 

In  the  capillaries  of  the  congested  organs,  the  blood  cor- 
puscles   contain    many    more    parasites. 
Smith  has  noted  in  one  case  from  2  to  3 
per   cent  of    infected    corpuscles   in    the 
^-^p=^r\^^  circulating  blood  but  in  cover- glass  prep- 

'"'xv-=rik?^C^  arations     made     at    the    autopsy    quite 

different  results  were  obtained.  In  those 
from  the  skeletal  muscles,  blood  of  the 
right  heart,  and  blood  from  the  bone 
marrow  (sixth  rib)  very  few  infected 
corpuscles  were  found  ;  in  the  blood 
from  the  left  heart  and  lung  tissue  from 
2  to  3  per  cent  of  infected  corpuscles  ;  in 
the  spleen  5  per  cent  ;  in  the  liver  and 
kidney  tissue   from   10   to   20  per  cent  ; 

and  in  the  hyperemic  fringes  of  the  omentum  and  the  heart 

muscle  50  per  cent  of  the  corpuscles 

were   infected.       In    other   cases   the 

blood    corpuscles    in     the    capillaries 

were    more    and    in    still    others    less 

extensively  infected.       In    the   living 

blood  the  parasites  were  pyriform,  but 

in    the   post-mortem    specimens   they 

were  more  nearly  round.      In  the  mild 

type  of  the  disease  from   5   to  50  per 

cent  of  the  red  corpuscles  in  the  circu- 
lation are  infected  for  a  period  of  from 

one  to  five  weeks.     The   parasite   is 

round  (coccus   form).     In    the    fresh 

preparations  it  is  seldom  seen  :  rarely 

it  can  be  detected  as  a  pale  spot  about 

0.5/1  in  diameter  at  the  periphery  of 

the  corpuscle.     In  stained  (alkaline  methylene  blue)  prepara- 
tions, the  parasites  appear  as  round  coccus-like  bodies  from 


Fig.  92.  Cover -glass  prep 
a ra tionfro m  k idn ey '.  Cor- 
puscles sfiocving  Piroplas- 
tna,  coccus  form  (Smith). 


INl'KCTION 


355 


Fig. 93.  Blood 
in  capillary  of 
heart  s/iorcj- 
ing  Piroplas- 
ma  {Siiiilh). 


0.2  to  0.5// in  diameter.  They  are  situated  within  the  cor 
puscle  on  its  border.  As  a  rule  only  one  is  found  in  i 
corpuscle.  Sometimes  a  division  was  evident 
separating  the  parasite  into  two  parts.  They 
must  be  differentiated  from  somewhat  similar 
looking  bright  bodies  which  are  seen  in  the  cor- 
puscles of  healthy  blood  during  different  seasons 
of  the  year. 

Concerning  the  life  history  of  this  parasite, 
Smith  considered  the  intraglobular  stage  hypo- 
thetically  the  swarming  stage,  which  precedes 
the  peripheral  coccus-like  bodies  and  the  pyri- 
form  and  spindle  shaped  bodies  which  develop 
from  the  divided  coccus-like  peripheral  forms. 
The  free  bodies  are  the  parasites  set  free  after 
they  have  reached  the  preceding  stage  by  disintegration  of 
the  infected  corpuscles.  They  are  most  commonly  found  in 
the  kidney.  The  reproduc- 
tive stage  has  not  been  recog- 
nized. 

§  268.  Infection.  Al- 
though practical  stockmen 
had  long  looked  upon  the 
tick  as  a  source  of  infection, 
it  remained  for  Smith  and 
Kilborne  to  experimentally 
demonstrate  that  so  far  as 
known  the  cattle  tick  {Bo'dphi- 
lus  annulatusY^  is  the  sole  carrier  of  the  parasite.  It  was 
pointed  out  by    them  that   when   southern   cattle   were  freed 

*This  tick  was  first  described  by  C.V.  Riley  in  1868  as  Ixodes  hovis. 
Later,  Cooper  Curtice  investigated  this  parasite  (Biology  of  the  Cattle 
Tick,  Journ.  Comp.  Med.  and  Veterinary  Archives,  July,  1891,  Jan., 
1892)  and'gave  it  the  generic  name  of  Boophilus  {o^  loving).  This 
seems  to  be  the  only  genus  of  cattle  ticks  which  transmits  the  parasite 
of  Texas  fever.  Recently  Karsch's  genus  Margaropiis  has  been  pro- 
posed as  the  correct  name  instead  of  Boriphilus. 


Fig.  94.  Sexually  mature  male 
tick  after  the  last  moult,  dorsal 
vieiv  (S)nith). 


356 


TEXAS    FEVER 


from  ticks  they  would  not  when  kept  together  in  small 
enclosures  transfer  the  disease  to  susceptible  animals,  but  that 
when  susceptible  cattle  become  infested  with  the  ticks  either 
by  grazing  in  infested  pastures  or  by  having  placed  upon  them 
young  ticks  hatched  in  the  laboratory  the  disease  appeared. 
The   infection  of    northern    cattle    with    Texas    fever   bv 


Fig.  95.     Photograph    of  animal    sick    with     Texas  fever.     {Photo- 
graphed by  Connaway). 

southern  animals  consists  therefore  in  first  infesting  them  with 
the  cattle  tick.-'-  The  number  of  ticks  necessary  to  carr}'  the 
disease  is  small  so  that  frequently  they  will  not  be  observ^ed 
unless   the   sick    animals   are   carefully   examined.     The   life 

*It  is  interesting  to  add  the  results  of  an  experiment  conducted  by 
Dr.  Cooper  Curtice  in  the  Bureau  of  Animal  Industry  which  shows  the 
necessity  of  the  tick  in  inoculating  cattle.  In  a  tick  infested  district  in 
the  south,  a  field  was  cleared  of  ticks  by  fencing  and  keeping  cattle  off 
for  a  year.  Susceptible  northern  cattle  were  transported  to  and  placed 
in  this  field  where  they  thrived  for  a  season.  The  second  year  they 
were  placed  in  a  second  cleared  pasture  where  they  kept  well  for  an- 
other year.  The  third  year  they  were  placed  in  a  tick  infested  pasture 
where  they  died  promptly  of  Texas  fever. 


INFECTION 


357 


cj'cle  of  the  tick  will,  therefore,  explain  the  variation  in  the 
time  elapsing  between  the  exposure  of  northern  to  southern 
cattle  and  the  appearance  of  the  disease.  Starting  with  tick 
infested  animals  placed  with  native  cattle  in  a  northern  pasture 
the  adult  female  ticks  drop  to  the  ground  almost  daily,  so  that 
the  following  life  cycle  may  be  assumed  to  begin  at  once. 

1.  Adult  ticks  drop  to  the  ground   in   from    i    to   3  days 
after  the  infested  cattle  are  placed  in  the  field. 

2.  Adult  ticks  lay  their  eggs  in  about  7  days  after   drop- 
ping to  the  ground. 

3.  Eggs  are  hatched  in  about  20  days  after  they  are  laid.-'^ 

4.  Young  ticks 
crawl  upon  cattle  from 
I  to  several  days  after 
they  are  hatched. 

5.  In  about  ten 
days  from  the  time  the 
young  ticks  crawl  upon 
the  susceptible  cattle  the 
rise  of  temperature  ap- 
pears. 

The  length  of  time 
that  must  elapse  (period 
of  incubation)  from  the 
exposure  of  susceptible  cattle  to  the  development  of  the 
disease  depends  on  whether  or  not  the  whole  life  cycle  of  the 
tick  must  be  passed  or  part  of  it  has  already  gone  by.  If 
susceptible  animals  are  placed  in  a  pasture  where  the  young 
ticks  are  just  ready  to  crawl  upon  them  the  infection  of  the 
cattle  is  accomplished  at  once  and  the  high  fever  appears  in 
about  ten  days,  practically  the  minimum  time.  It  has  been 
experimentally  demonstrated  that  the  young  ticks  are  able  to 
travel  for  a  considerable  distance  in  a  pa.sture.  In  pastures 
where  tick  infested  cattle   are   grazing,  young  ticks  are  very 

*Mohler  states  that  the  time  required  for  the  hatching  varies  from 
13  days  to  six  weeks,  depending  upon  temperature,  moisture,  soil,  etc. 
He  states  further  that  the  eggs  may  remain  dormant  for  several  months. 


Fig.    96.     Sc.vHally    Dialure  fcina/e  after 
the  last  Dioitlt ,  dorsal  viezv  {Siiiit/i). 


,58 


TEXAS    FEVER 


liable  to  be  on  the  ground  continuously.  In  estimating  the 
time  to  elapse  after  the  exposure  to  the  tick  infested  field, 
before  the  disease  will  appear,  it  is  necessary,  therefore,  to 
determine  the  exact  stage  in  the  life  cycle  of  the  ticks  at  the 
time  when  the  animals  come  in  contact  with  them. 

Small  quantities  of  the  blood  from  immunized  cattle  in 
the  tick  infested  district,  when  injected  into  susceptible 
animals  either  intravenously  or  beneath  the  skin,  will  produce 
the  disease.  While  this  mode  of  infection  rarely  if  ever 
occurs  in  the  natural  order^of  events,  it  may  happen  that  in 

case     of     certain 


0 


Fig.  97. 


Eggs  and  you  Jig  tick 
(Smit/i). 


/Ksi    liatclied 


operations  bits  of 
blood  may  be  car- 
ried directly  from 
a  southern  to  a 
northern  animal 
thus  inoculating 
the  latter  with  the 
disease. 

In    the  fall  of 

1898  two  cases  occurred  in  the  practice  of  Dr.  Ambler  of 
Chatham,  N.  Y.  The  owner  had  his  animals  dehorned  in 
December  and  soon  afterward  two  fatal  cases  of  Texas  fever 
developed.  The  Piroplasma  and  the  characteristic  lesions 
were  present.  Inquiry  revealed  the  interesting  fact  that  the 
two  animals  which  .sickened  and  died  were  dehorned  immedi- 
ately after  two  imported  southern  cattle.  The  owner  was  not 
aware  of  the  fact  at  the  time  that  these  were  southern  bred 
cattle,  as  he  had  bought  them  of  a  dealer  in  Vermont.  More 
recently  another  case  of  this  disease  produced  in  the  same  way 
has  been  reported. 

§  269.  Symptoms.  In  the  acute  type  of  the  disease 
which  occurs  during  the  hot  summer  months,  the  onset  is  sud- 
den and  usually  all  animals  exposed  to  the  same  infection 
together  come  down  at  the  same  time.  The  first  indication  of 
the  disease  is  a  rise  of  temperature,  at  first  higher  in  the  after- 


SYMPTOMS  359 

noon  than  morning,  but  this  oscillation  is  minimized  later  in 
the  course  of  the  disease  when  the  temperature  remains  high. 
The  temperature  rarely  rises  above  107°  F.  With  a  clinical 
thermometer  the  temperature  can  be  detected  two  or  more 
days  before  there  are  other  symptoms.  The  respiration  may 
rise  to  between  60  and  100  and  the  pulse  may  range  between 
80  and  1 10  per  minute.  Late  in  the  disease  there  may  be 
hemoglobinuria.  Smith  and  Kilborne  found  it  in  33  out  of  46 
fatal  cases  in  which  urine  was  found  in  the  bladder.  The 
passing  ot  the  colored  urine  before  death  was  noted  in  but  four 
of  their  cases.  In  one  of  these  which  showed  hemoglobinuria 
four  days  before  death,  the  urine  in  the  bladder  was  clear  at 
post-mortem.  As  this  condition  seems  to  depend  upon  the  ra- 
pidity of  the  destruction  of  the  red  blood  corpuscles,  a  slow  dis- 
integration may  enable  other  organs  to  dispose  of  the  coloring 
matter,  while  in  rapid  destruction  of  the  blood  much  of  it  may 
be  thrown  into  the  urine.  The  urine  contains  small  quantities 
of  albumin.  At  first  the  specific  gravity  may  be  high  but 
later  it  ranges  from  loio  to  1020  and  fails  to  effervesce  with 
acids.  The  color  varies  according  to  the  quantity  of 
hemoglobin.  As  a  rule  there  is  marked  constipation  during 
the  high  fever.  There  is  loss  of  appetite  and  usually  cessation 
of  rumination  with  the  high  fever.  The  blood  is  thin  and 
pale.  The  high  temperature,  hemoglobinuria  and  thinness  of 
the  blood  are  quite  diagnostic  symptoms  of  the  acute  type. 

The  course  of  the  disease  may  vary,  but  the  continuous 
high  temperature  does  not  usually  last  for  more  than  ten  days. 
Death  often  intervenes  in  from  five  to  eight  days.  In  the 
mild,  nonfatal  or  chronic  type  which  was  first  pointed  out  by 
Smith  and  Kilbourne  and  which  occurs  in  the  late  summer  or 
autumn,  the  general  symptoms  are  similar  to  those  of  the 
acute  type  except  they  are  not  so  severe  and  are  prolonged  for 
a  greater  length  of  time.  The  parasite  is  of  the  .spherical  or 
coccus  form.  The  general  symptoms  are  not  manifested  unless 
the  temperature  goes  above  103°  F.  Hemoglobinuria  is  not 
observed  in  this  type.  Cattle  which  have  passed  through  an 
acute  type  owing  to  the  heated  season  may  have   a   relapse   in 


360  TEXAS    FEVER 

the  form  of  a  mild  type  in  the  fall.  The  essential  difference 
between  the  two  types  is  found  in  the  different  stages  of  the 
parasite  circulating  in  the  blood.  Unless  the  temperature  is 
taken  and  the  blood  carefully  examined,  mild  types  of  Texas 
fever  would  be  either  overlooked  or  mistaken  for  any  one  of  a 
variety  of  disorders  common  among  cattle. 

§  270.  Morbid  anatomy.  Cattle  which  die  of  Texas 
fever  undergo  post-mortem  changes  very  rapidly.  For  this 
reason  the  description  of  lesions  made  some  hours  after  death 
may  be  misleading. 

Externally  the  animal  presents  nothing  abnormal  or  char- 
acteristic of  the  disease.  Rarely  dried  bits  of  blood  may  be 
found  and  also  some  small  slightly  elevated  areas  of  a  bluish 
color.  The  skin  between  the  thighs,  upon  and  about  the 
udder  and  possibly  elsewhere  may  have  cattle  ticks  attached. 
It  is  important  under  ordinary  circumstances  to  look  for  this 
parasite.  The  subcutaneous  tissue  may  be  more  or  less  yellow 
in  color.  Edema  of  the  subcutis  over  the  ventral  portion  of 
the  body  has  been  observed.  The  muscles  are  usually  normal 
in  appearance  although  frequently  they  are  pale. 

Very  slight  if  any  lesions  have  been  recorded  as  occurring 
in  the  central  nervous  system  and  lungs.  Blood  extravasa- 
tions usually  occur  beneath  the  skin  and  endocardium,  espe- 
cially of  the  left  ventricle.  On  the  external  surface  the 
petechiae  occur  for  the  greater  part  along  the  intraventricular 
"groove  near  the  base.  The  capillaries  of  the  heart  muscle  are 
packed  with  corpuscles.  Parenchymatous  and  fatty  degene- 
ration of  the  muscular  fibers  sometimes  exists.  The  right  ven- 
tricle is  distended  with  blood  either  fluid  or  clotted  and  the 
left  one  firmly  contracted. 

In  the  abdominal  cavity  there  are  frequent  edematous 
areas  about  the  kidneys  and  in  the  portal  regions  between  the 
duodenum  and  liver.  The  omentum  is  often  sprinkled  with 
peculiar  hyperemic  patches  consisting  of  delicate  shreds  of 
vascular  tissue.  This  condition,  however,  is  not  characteristic 
of  Texas  fever. 


MORBID    ANATOMY  36 1 

Usually  the  most  conspicuous  changes  are  in  the  spleen. 
This  organ  is  much  enlarged  and  increased  from  two  to  four 
times  its  normal  weight.  The  normal  markings,  Malpighian 
bodies  and  trabeculae,  are  hidden  in  the  dark  brownish -red, 
glistening  pulp  which  distends  the  capsule.  The  pulp  may  be 
firm  or  it  may  be  in  a  semi-fluid  condition  so  that  it  oozes  out 
if  the  surface  is  cut.  The  enlargement  and  color  of  the  spleen 
are  due  to  an  engorgement  of  red  blood  cells.  There  may 
also  be  present  a  greater  or  less  number  of  large  cells  contain- 
ing granules,  red  corpuscles  or  clumps  of  3'ellowish  pigment. 
Free  pigment  is  much  more  abundant  than  it  is  in  healthy 
spleens. 

The  liver  is  extensively  affected.  It  is  enlarged,  con- 
gested, edges  rounded,  the  bile  ducts  more  or  less  distended 
and  the  parenchyma  is  usually  in  a  state  of  fatty  degenera- 
tion. The  color  is  paler  than  normal  and  usually  the  surface 
is  somewhat  mottled.  On  section  the  color  of  the  cut  surface 
is  brownish-yellow  or  it  may  be  mottled  like  the  surface.  The 
mottling  is  due  to  a  discoloration  owing  to  degeneration  of  a 
zone  bordering  the  intralobular  vein.  This  zone  varies  in 
width  and  its  peculiar  color  seems  to  be  due  to  a  tendency  to 
necrosis.  It  is  characterized  b\'  parenchymatous  degeneration 
and  the  loss  of  the  nucleus.  It  may  involve  a  third  or  more  of 
the  lobule.  This  portion  stains  very  feebly  or  not  at  all.  The 
explanation  for  the  necrosis  of  the  liver  cells  is  suggested  by 
Smith  as  being  due  to  the  plugging  up  of  the  ultimate  bile 
ca.nals  with  solid  bile  which  may  interfere  in  some  way  with 
the  nutrition  of  the  adjacent  liver  cells.  The  bile  stasis  he 
considers  as  a  result  of  the  breaking  up  in  the  capillaries  of 
the  liver  of  enormous  numbers  of  infected  corpuscles.  This 
results  in  an  abnormal  fluid  containing  an  excess  of  solids 
which  the  bile  ducts  are  unable  to  carry  away.  When 
examined  in  fresh  condition  or  in  sections  of  tissue  fixed  in 
Miiller's  fluid  the  engorgement  of  the  bile  canaliculi  is  seen. 
The  bile  stasis  may  occur  over  a  portion  or  a  whole  of  the 
lobule.  The  gall  bladder  contains  usually  an  abnormal  quan- 
tity of  changed  bile.      It  is  thick  and  often  semi-solid  in  con- 


362  TEXAS    FEVER 

sistency,  holding  in  suspension  many  flocculi.  It  imparts  a 
deep  yellowish  tinge  to  all  articles  coming  in  contact  with  it. 
Owing  to  the  mucus  which  is  present  it  is  quite  viscid. 

The  changes  in  the  kidneys  vary.  If  death  occurs  early 
they  are  usually  enlarged  and  uniformly  darker  than  normal 
throughout.  The  capillaries  are  distended  with  red  corpus- 
cles. Parenchymatous  and  fatty  degenerations  are  not  com- 
mon, although  occasionally  present  in  the  epithelium  of  the 
tubules.     The  pelvis  is  often  sprinkled  with  ecchymoses. 

The  bladder  may  contain  ecchymoses. 

It  is  important  to  note  that  throughout  the  kidneys,  liver 
and  spleen  pigment  may  be  more  or  less  abundant. 

In  the  digestive  tract  the  lesions  of  this  disease  consist 
largely  of  congestion  of  the  mucosa  especially  in  lines  corre- 
sponding to  the  summits  of  the  folds  of  the  mucous  membrane. 
It  is  more  marked  in  the  cecum  and  rectum  than  in  the  colon. 
The  cecum  and  less  often  the  rectum  contain  dry,  hard  fecal 
balls.  In  some  cases  in  the  intestines  lesions  are  not  observable. 
In  the  older  writings  much  emphasis  is  placed  on  certain 
lesions,  mostly  nodular  or  abrasions,  in  the  digestive  tract. 
Smith  has  shown,  however,  that  most  of  these  are  due  to 
animal  parasites  and  have  no  relation  to  Texas  fever. 

As  already  stated,  Texas  fever  is  a  disease  of  the  blood 
and  consequently  it  is  in  this  fluid  that  the  most  constant  and 
morbid  changes  occur.  They  are  characterized  by  the  blood 
becoming  thin  and  watery  with  a  destruction  of  the  red  blood 
corpuscles.  In  some  of  the  cases  the  loss  of  corpuscles  is  rapid 
and  continuous  until  death  or  convalescence,  while  in  others 
there  is  a  marked  oscillation  between  destruction  and  regenera- 
tion. In  some  animals  the  loss  is  not  continuous,  but  the 
course  of  the  disease  is  marked  by  the  periods  of  rapid  blood 
destruction  and  periods  of  rest,  or,  as  it  were,  where  the  blood 
destruction  was  holding  its  own.  These  points  are  best  illus- 
trated from  actual  cases,  three  of  which  are  taken  from  the 
report  by  Smith  and  Kilborne. 


MORBID    ANATOMY 


363 


(No 

.  129) 

(No. 

142) 

(No, 

•56) 

Date. 

No.  of 
Corpuscles. 

Date. 

No.  of 
Corpuscles. 

Date. 

No.  of 
Corpuscles. 

Axig.   II, 

6,125,000 

Sept. 

16, 

6,890,000 

Sept. 

20, 

6,844,000 

13. 

7,171,000 

22, 

5,430,900 

22, 

5,640,000 

16, 

5,370,000 

24, 

4,562,000 

29. 

2,307,0.0 

27, 

3,310.000 

29- 

5,274,000 

Oct. 

9, 

5,436,000 

29. 

1,675,000 

Oct. 

4, 

3,902,000 

22, 

4,666,000 

30, 

Died  8  p.m. 

1 

8. 

5,983,000 

25, 

2,754,000 

1 

22, 

4,333,000 

30, 

2,720,000 

First  hi.ii 

^h  a.:m.  temp 

Nov. 

4. 

5,586,000 

Nov. 

6, 

2,344,000 

Aug.  24. 

\ 

1 

8, 
13, 

1 ,984,000 
1,183,000 

As  evidence  of  the  diminution  of  the  number  of  corpuscles 
within  the  body  these  authors  point  ( i  )  to  the  loss  of  hemo- 
globin through  the  kidneys,  (2)  to  the  overproduction  of  bile 
which  is  abnormal  in  the  abundance  of  pigment  and  (3)  to  the 
actual  observation  of  their  destruction  by  the  micro-parasite 
under  the  microscope. 

The  regeneration  of  blood  corpuscles  is  indicated  perhaps 
by  the  count,  but  more  surely  by  the  forms  of  the  corpuscles 
themselves.  The  abnormal  forms  are  the  very  large  corpus- 
cle.s,  "punctate"  forms  and  lastly  the  diffuse  stained  or 
"tinted"  forms  and  the  erythroblasts.  The  first  of  these 
may  appear  when  the  blood  count  reaches  3,000,000  and  the 
other  forms  when  it  is  still  lower.  These  various  forms,  how- 
ever, are  probably  embryonic  or  immature  corpuscles,  which 
are  forced  prematurely  into  the  circulation  by  the  blood  pro- 
ducing organs  in  trying  to  overcome  the  rapid  destruction  of 
corpuscles  by  the  parasite.  The  action  of  the  disease  upon 
the  leucocytes  or  the  defensive  activities  of  the  white  corpus- 
cles in  combating  the  parasite  of  Texas  fever  have  not  been 
determined.  In  the  work  thus  far  performed  and  reported, 
they  have  received  little  attention.  Suffice  it  to  say  that  they 
have  not  been  in  evidence  in  this  conflict  and  probabl>-  take 
little  or  no  part  in  the  morbid  changes  of  Texas  fever. 

§  271.      Differential    diagnosis.     Texas   fever  is    easih^ 


364  TEXAS    FEVER 

differentiated    from  other  disorders  of  infectious   diseases  by 
the  presence  of  its  specific  parasite. 

In  the  absence  of  a  suitable  microscope  the  differentiation 
can  in  most  cases  be  made  from  the  character  of  the  lesions, 
the  history  of  the  animals,  the  presence  of  the  cattle  tick  and 
the  course  of  the  disease.  The  lesions  are  not  simulated  by 
any  other  disease  of  cattle,  although  the  enlarged,  dark  spleen 
may  suggest  anthrax  and  in  a  hasty  diagnosis  the  two  may  be 
contused.  From  the  fact  that  all  animals  exposed  together  us- 
ually come  down  with  the  disease  together  poisoning  may  be 
suggested,  but  here  again  a  study  of  the  symptoms  and  lesions 
are  sufficient  to  eliminate  toxic  disorders. 

§  272.  Prevention.  Thediscoveryofthespecificcau.se 
of  Texas  fever  and  of  the  cattle  tick  as  the  common  means  of 
its  transmission  has  reduced  the  preventive  measures  to  a 
direct  warfare  against  the  tick.  The  National  government 
has  determined  the  territory  in  which  the  tick  naturally  exists 
and  from  which  cattle,  on  account  of  the  parasite,  cannot  be 
shipped  to  uninfected  districts,  except  under  certain  very  re- 
stricted conditions.  (See  regulations  for  transmission  of  cattle, 
p.  618,  Report  of  the  Bureau  of  Animal  Industry  for  1898). 
Likewise  susceptible  northern  cattle  cannot  be  transported  to 
the  infested  districts  (.south  of  Texas  fever  line)  unless  they 
can  be  placed  in  fields  that  have  been  freed  from  ticks.  The 
elimination  of  the  disease  depends  therefore  upon  the  elimina- 
tion of  Boophilus  ammlatus.  Recently  the  government  has 
undertaken  to  eliminate  the  ticks.  Thus  far  the  reports  are 
most  encouraging.  There  seems  to  be  no  reason  why  in  the 
dairy  districts  of  the  South  their  eradication  cannot  be  accom- 
plished. 

^  273.  Immunizing  susceptible  cattle.  A  number  of 
investigations  have  been  undertaken  directed  toward  the  de- 
velopment of  methods  for  immunizing  northern  cattle  against 
Texas  fever  in  order  to  enable  the  shipment,  especially  of 
breeding  stock,  into  the  South.  In  1895,  the  writer  in  con- 
junction with  Schroeder,  began  an  immunizing  experiment 
which  was  continued  and  reported  by  Schroeder  in  1898. 


IMMUNIZING    CATTLE 


365 


Young  animals  were  selected  and  injected  with  blood 
taken  directly  from  the  jugular  veins  of  southern  animals. 
The  injections  were  made  in  the  fall  and  winter  and  in  the 
spring  the  animals  were  placed  in  a  highly  infected  field  at 
Manchester,  Va.,  where  they  remained  for  the  summer.  Dur- 
ing this  time  they  were  under  the  immediate  observation  of 
Curtice,  who  made  a  careful  study  of  the  blood,  temperature 
and  extent  of  tick  invasion.  The  results  of  this  experiment 
are  shown  in  Schroeder's  tabulation,  which  is  appended.  The 
animals  were  again  exposed  the  following  season  without  the 
development  of  Texas  fever. 


Animal 

Effect  of 

Effect  of  the 

No. 

blood  injection. 

exposure  to  cattle  ticks. 

I 

Severe. 

Very  mild  disease. 

2 

" 

Well  marked  but  mild. 

3 

Very  severe. 

Very  mild. 

4 

" 

No  disease. 

5 

Mild. 

"         " 

6 

" 

Very  mild. 

7 

Severe. 

No  disease. 

8 

" 

" 

9 

Control  Animals. 

"         " 

10 

Died  June  20. 

II 

"      July  9. 

12 

"      June  26. 

13 

"      July  9- 

14 

Very  severe  disease,  recovered. 

The  inoculation  disease  appears  in  from  eight  to  ten  days 
after  the  injection  of  the  blood.  It  lasts  from  one  to  two 
weeks.  The  symptoms  are  occasionally  of  a  still  shorter  dura- 
tion, but  the  altered  condition  of  the  blood  persists  in  some 
cases  for  a  much  longer  period. 

Dairy mple,  Dod.son  and  Morgan,  of  the  Louisiana  Ex- 
periment Station,  conducted  experiments  along  this  line. 
They  showed  that  immunity  against  a  fatal  attack  of  Texas 
fever  can  be  conferred  on  susceptible  cattle  by  inoculation  with 
the  blood  of  a  native  vSouthern  animal  or  one  which  has  recentlj^ 
been  rendered  immune. 


366  TEXAS    FEVHR 

The  Experiment  Station  of  that  state  offers  to  immunize 
(free  of  charge)  northern  cattle,  if  they  are  shipped  to  the 
state,  for  its  stock  raisers. 

In  Missouri,  Counaway  has  immunized  a  few  animals  with 
the  blood  serum  from  immune  (southern)  cattle.  In  Missis- 
sippi, Robert  has  tried  the  serum  for  both  prevention  and 
treatment  with  somewhat  similar  results.  In  Virginia  and 
Oklahoma  the  disease  and  its  prevention  have  been  studied. 
In  Texas,  Francis  is  immunizing  cattle  with  most  excellent 
results.  He  has  pointed  out  the  value  of  immunizing  young 
(2  to  6  weeks  old)  calves  by  artificially  infesting  with  ticks. 
In  Australia  the  problem  of  immunizing  cattle  against  the 
effects  of  the  spreading  of  the  cattle  tick  in  order  to  save  their 
stock  from  "tick  fever"  has  become  a  matter  of  serious  con- 
sideration. Certain  European  writers  claim  that  immunity 
can  not  be  permanently  induced  by  artificial  injections. 
Schroeder  has  shown  that  the  parasite  remains  virulent  in  the 
blood  of  naturally  immunized  cattle  for  from  10  to  12  years. 

The  very  limited  knowledge  of  the  life  cycle  of  the  para- 
site of  Texas  fever  precludes  a  satisfactory  explanation  ot  the 
modus  operandi  in  the  production  of  immunity  by  these  various 
procedures.  On  this  point  there  is  need  for  much  extended 
investigation. 

REFERENCES. 

1.  Babes.  Die  Aetiologie  der  seucheuhaften  Haemoglobiuurie 
des  Rindes.      Virc/iozv's  Arcliiv,  Jan.  1889,  .S.  81. 

2.  CONNAWAY.  Texas  fever  or  acclimation  fever.  Bullet  in  No. 
37.     Mo.  State  Board  of  Agriculture,  1897. 

3.  Dalrymple,  Morgan  and  Dodson.  Texas  or  southern  cattle 
fever.     Bulletin  5/.     Louisiana  Agric.  Expt.  Station,  1898. 

4.  DiNWiDDiE.  Some  Texas  fever  experiments.  Bulletin  No.  20 
Ark.  Agric.  Exper.  Station,  1893. 

5.  Francis  and  Connawav.  Texas  fever.  Bulletin  No.  jj. 
Texas  Agric.  Expt.  Station,  1899. 

6.  Gamgee,  Dodge,  Bii,r.iNGS  AND  Curtis.  Diseases  of  cattle  in 
the  United  States.  Report  of  the  Commissioner  of  Agriculture,  Wash- 
ington, D.  C,  1871. 


RKKERKNCKS  367 

7.  Hughes.  The  fi^ht  against  Texas  Fever.  A  review  of  the 
work  being  attempted  in  the  south  for  the  control  and  eradication  of 
the  disease.     Am.  Vet.  Review,  Vol.  XXIX  (  1906),  p.  1309. 

8.  Hunt  .\nd  Coi^mns.  Report  on  lick  fever.  Brisbane.  (Jueens- 
land,  Australia,  1899. 

9.  Koch.  Vorlaufiger  Bericht  iiber  das  Rhodesische  Rotwasser 
oder  "  Afrikanische  Kustenfieber."  Archiv.  fi'ir  wiss.  u.  praktische 
Tier/ieilkundc,  Bd.  XXX  (1904)  S.  281. 

10.  Lewis.  Texas  fever.  Bulletin  No.  S9-  Oklahoma  Agric. 
Exper.  Station,  1899. 

11.  LiGNlKRES.  La  "Tristeza"  on  Malarie  Bovine  dans  la  Repub- 
liqne  .\rgentina.     Buenos  Aires,  1890.      (Full  bibliography). 

12.  Mavo.  Texas  fever.  Bulletin  No.  dc).  Kan.  Agric.  Exper. 
Station,  1897. 

13.  McCuLLOCH.  The  prevention  of  Texas  feverand  the  amended 
laws  controlling  contagious  disease.  Bulletin  No.  104.  Virginia  Agric. 
Exper.  Station,  1899. 

14.  MOHLER.  Texas  Fever.  Bulletin  No.  jS.  Bureau  0/  Animal 
Industry,  1905. 

15.  NiLES.  Splenetic  or  Texas  cattle  fever.  Bulletin  No.  61,. 
Virginia  Agric.  Exper.  Station,  1896. 

16.  NoRGAARD.  Dipping  cattle  for  the  destruction  of  ticks. 
Annual  Report,  Bureau  of  Animal  Industry,  1895-6,  p.  109. 

17.  Paouin.  Texas  Fever.  Bulletin  No.  11.  Mo.  Agric.  Exper. 
Station,  1890. 

18.  S.4lLMOX.  Contagious  diseases  of  animals.  Special  report  No. 
22,  Washington,  D.  C. 

19.  Salmon.     Report  Commissioner  of  Agriculture.    1881-2. 

20.  Salmon.  Annual  Reports,  Bureau  of  Animal  Industry. 
1884-5. 

21.  SCHROEDER.  Inoculation  to  produce  immunity  from  Texas 
fever  in  Northern  cattle.     Ibid.     1898,  p.  273. 

22.  vSCHROEDER.  Notes  on  cattle  tick  and  Texas  fever.  Annual 
Report  of  the  Bureau  of  Animal  Industry,  1905.  p.  49. 

23.  SCHROEDER  AND  CoTTON.  Persistence  of  Texas  fever  or- 
ganism in  blood  of  southern  cattle.     Ibid.,  p.  71. 

24.  Smith.  Preliminary  observations  on  the  microiirganism  of 
Texas  fever.      The  Medical  News.     Dec.  21,  18S9. 

25.  Smith  and  Kilborne.  Texas  fever.  Bulletin  No.  i. 
Bureau  of  Animal  Industry,  U.  S.  Dept.  Agriculture,  1893. 


368  ICTERO-PIEMATURIA 

26.  vSmith  and  Kilborne.  Annual  Report,  Bureau  of  Aniutal 
Industry,  1891-2.     {Issued  iSg^). 

27.  Stiles.     Report  New  York  State  Board  of  Health,  1868. 

28.  Stockman.  Some  points  to  be  considered  in  connection  with 
Rhodesian  redwater.  Jour.  Comp.  Path,  and  Thera.,  Vol.  XVIII 
(1905),  p.  64. 

29.  TheilER  and  Stockman.  Some  observations  and  experi- 
ments in  connection  with  Tropical  bovine  piroplasmosis  (East-coast- 
fever  or  Rhodesian  Redwater).  Jour.  Comp.  Path,  and  Thera. ,Vo\. 
XVII  (1904),  p.  193. 


ICTERO-HEMATURIA  IN  SHEEP 

Synonyms.  Carceag  ;  hemaglobinuria  in  sheep  ;  Piro- 
plasmosis in  sheep. 

§  274.  Characterization.  This  is  an  enzootic  disease 
characterized  by  a  rise  of  temperature  with  chill,  and  later 
icterus  and  marked  changes  in  the  blood  due  to  a  specific  para- 
site invading  its  red  blood  corpuscles. 

§  275.  History.  In  1892,  Babes  pointed  out  the  con- 
stant presence  of  an  intraglobular  parasite  in  the  blood  of 
sheep  suffering  from  an  enzootic  hemoglobinuria  in  Roumania. 
Bonome  studied  the  same  affection  in  Italy  in  1895.  Williams 
described  this  disease  in  Montana  in  the  same  year.  He  did 
not,  however,  report  the  finding  of  the  parasite  or  record  its 
description. 

§  276.  Geographical  distributions.  The  piroplasma 
infection  of  sheep  has  been  found  in  several  places  in  Europe. 
Its  existence  in  the  United  States  is  in  question,  although  the 
description  given  by  Williams  of  the  disease  he  found  suggests 
very  strongly  a  Piroplasma  origin. 

§  277.  Etiology.  Pii'oplasma  avis  is  the  specific  cause. 
This  organism  is  very  clo.sely  related  to  Piroplasma  bigemimini 
of  Texas  fever. 

§  278.     Symptoms.     At   the   beginning    the    symptoms 


EOUINE    MALARIA  369 

are  said  to  be  severe.  There  is  a  rise  of  temperature  usually 
with  a  chill.  After  one  or  two  days  icterus  appears.  The 
urine  is  occasionally  of  a  reddish  brown  color,  due  to  the 
presence  of  hemoglobin.  Death  is  preceded  by  a  collapse  in 
which  the  temperature  is  subnormal.  The  duration  of  the 
disease  is  usually  but  a  few  days. 

§  279.  Morbid  anatomy.  The  subcutaneous  tissues 
are  infiltrated  with  a  yellowish  colored  liquid.  The  blood  is 
thin  and  watery.  The  muscles  are  pale  and  edematous.  The 
mucous  membranes  of  the  pharynx  and  intestines  are  often 
hemorrhagic.  The  liver  is  small,  soft  and  yellowish  in  color. 
The  spleen  is  usually  slightly  enlarged.  The  kidneys  are  soft 
and  friable.     There  usually  occurs  a  parenchymatous  nephritis. 

§  280.  Differential  diagnosis.  This  disease  is  posi- 
tively diagnosed  by  finding  the  piroplasma  in  the  blood.  It  is 
to  be  differentiated  from  anthrax,  in  which  the  specific  organ- 
ism is  readily  found  in  the  blood  and  organs. 

REFERENCES 

1.  Babes.  L'etiologie  d'une  enzootic  des  moutons  denommee 
Carceag  en  Roumanie.  Comp.  R.  del' Acad,  dcs  Sciences,  Vol.  CXV 
(1892),  p.  359. 

2.  BoNOME.  Uber  parasitiire  Ictero-Haeniaturie  der  Schafe,  Ein 
Beitrag  zum  Studium  der  Amobo-Sporidien.  Archiv.  fiir.  path. 
Atiatomie,  Bd.  CXXXIX,  S.  i. 

3.  Williams.  The  parasitic  Ictero-Haematuria  of  Sheep.  Bulletin 
No.  S,  3/oH.  Agric.  Exp.  Station,  iSg^,  also  Anier.  />/.  Reviezv,  1897, 
P-  377- 


EQUINE    MALARIA 

Syiiottyms.  Piroplasmosis  in  horses  ;  South  African 
horse  sickness  ;   "Biliary  fever." 

§  281.  Characterization.  This  affection  of  horses  is 
characterized  by  a  high  temperature  and  a  yellowish  tint  of  the 
mucous  membranes.  The  spleen  is  enlarged  and  the  blood 
contains  a  Piroplasma  eqiii. 


370  EQUINE    oNIALARlA 

§  282.  History.  The  disease  appears  to  have  been  first 
described  by  Wiltshire  in  18S3.  Guglielmi  discovered  the 
parasite  of  this  affection  in  1S99,  and  Rickmann  found  it  in  a 
large  number  of  horses  that  died  of  "horse  sickness."  A 
good  description  of  this  affection  was  given  by  Theiler  in  1901. 

^  283.      Geographical     distribution.  This       disease 

appears  to  be  very  largely  restricted  to  Southern  Africa  and 
Europe.  The  disease  known  as  malarial  fever  in  the  United 
States  has  not  been  demonstrated  to  be  due  to  a  piroplasma. 
Peters  describes  this  disease  in  horses  in  the  West  but  he  did 
not  find  its  specific  parasite. 

§  284.  Etiology.  Laveran  w^ho  has  studied  this  affection 
states  that  its  cause  is  Piroplasma  equi.  It  is  closeh'  related 
to  P.  bigeminum.  It  measures  from  0.5  to  2.0  //.  During  the 
invasion  and  multiplication  of  the  parasites  there  is  a  high 
temperature.  In  the  blood  corpuscle  the  parasite  is  single,  in 
pairs  or  in  rosette  form.  The  disease  was  believed  not  to  be 
transmitted  directly  with  the  blood  containing  the  parasite. 
Theiler,  however,  succeeded  in  proving  that  equine  piroplas- 
mosis  is  inoculable  with  the  blood  of  immune  horses  into  sus- 
ceptible ones.  The  natural  method  of  infection  is  not  known, 
but  it  is  believed  by  many  to  be  by  means  of  a  tick. 

Theiler's  conclusions  relative  to  the  transmissibility  of 
this  parasite  are  as  follows  : 

(i)  The  piroplasma  found  in  the  mule  and  the  donkey 
is  identical  with  the  piroplasma  equi  first  found  in  the  horse. 

(2)  The  disease  caused  by  this  piroplasma  is  inoculable 
with  blood  of  immune  animals  into  susceptible  ones  belonging 
to  the  domesticated  species  of  the  genus  eqiuis. 

(3)  The  horse  shows  the  greatest  susceptibility  for  this 
piroplasma  ;  the  donkey  is  less,  and  the  mule  the  least, 
susceptible. 

(4)  The  possibility  of  a  practicable  inoculation  against 
the  piroplasmosis  stands  in  the  reverse  order  of  the  suscepti- 
bility.    The    mule    may    be    safely    inoculated    with    immune 


IMORBin    ANATO:\IY 


371 


blood  of  any  of  the  three  respective  equities  ;  the  immune 
horse-blood  produces  the  severest  reaction,  the  immune  mule- 
blood  causes  little  reaction,  and  so  does  the  immune  donkey- 
blood. 

The  period  of  incubation  \s  stated  by  Theiler  to  be  21  days. 

§  285.  Symptoms.  An  acute  and  chronic  type  are 
recognized.  The  acute  type  begins  with  a  high  temperature. 
There  is  jaundice,  appearing  first  in  the  eyes.  Death  follows 
rapidh^  often  at  the  time  of  the  maximum  temperature.  In 
the  chronic  cases  the  symptoms  are  prolonged. 

77;<?  duration  of  the  disease  is  from  a  few  to  several  days. 

§  286.  Morbid  anatomy.  The  animal  is  emaciated. 
The  blood  is  said  to  be  thin  and  watery.  The  conjunctival 
subcutaneous  tissue  is  of  a  yellowish  color.  The  muscles  are 
of  a  reddish  brown.  All  of  the  tissues  are  anemic.  The 
spleen  is  very  large.  Theiler  has  found  the  spleen  to  be  twice 
the  normal  size.  The  lymphatic  glands,  especially  those 
of  the  spleen,  liver  and  kidneys,  are  tumefied  and  often  hemorr- 
hagic. The  liver  is  yellowish  in  color  and  engorged  with 
blood.  The  bile  capillaries  are  distended.  The  mucosa  of  the 
digestive  tract  is  pale,  or  sprinkled  with  reddish  areas.  The 
glands  in  the  thorax  are  enlarged  and  infiltrated  with  a  gela- 
tinous substance.  Occasionally  there  are  ecchymoses  on  the 
lungs  and  heart.  The  heart  muscle,  pericardium  and  valves  are 
frequently  infiltrated  with  a  gelatinous  substance.  The  blood 
clots  are  soft.  The  exuded  serum  is  of  a  yellowish  brown 
color.  The  parasites  are  found  in  all  parts.  Death  usually 
follows  an  acute  attack. 

§  287.      Differential  diagnosis.     Equine  malaria  is  to  be 

differentiated  from  (i)  Brustseuche,  (2)  Nagana,  and  (3) 
anthrax.  In  the  last  two  named  diseases  the  finding  of  the 
specific  organisms  will  determine  the  diagnosis.  The  finding 
o'i  Xht  piroplasinawiW  distinguish  it  horn  Brustseuche. 


372  CANINE    MALARIA 

REFERENCES. 

1.  BowHiLL.  Equine  piroplasmosis  or  "biliary  fever."'  The 
Jour,  of  Hygiene,  Vol.  V  (igosj.p.  7. 

2.  Dale.  Piroplasmosis  of  the  donkey.  Jour,  of  Coinp.  Path, 
and  Thera.,  Vol.  XVI  (1903),  p.  312. 

3.  GugliELmi.  Un  caso  di  malaria  del  cavallo.  Clinica  Veteri- 
iiaria,  1899,  p.  220. 

4.  Laverax.  Contributions  a  I'etude  de  Piroplasma  equi.  Comp. 
R.  de  la  Societe  de  biologie,  1901. 

5.  Peters.  Malaria  of  the  horse.  Nebraska  Agric.  Exp.  Sta- 
tion, Press  Bulletin  22. 

6.  Pricolo.  Beitrag  zur  Piroplasmose  des  Pferdes.  La  Clin. 
Vet.,  1906,  p.  529. 

7.  RiCKMANX.  Siidafrikanische  Pferdesterbe.  Berliner  iliie- 
rarztl.      Wochenschrift,  1902,  S.  4. 

8.  TheilER.  Die  Pferde-malaria.  These  de  Berne.  Schiveizer- 
Archiv  filr  Thierheilkunde,  1901,  S.  253. 

9.  Theiler.  Further  notes  on  Piroplasmosis  of  the  horse,  mule 
and  donkey.  Jour.  Comp.  Path,  and  Thera.,  Vol.  XVIII  (1905), 
p.  229. 


CANINE    MALARIA 

Synonyms.  Piroplasmosis  of  dogs;  malignaut  malarial 
jaundice;  malignant  jaundice  in  the  dog. 

§  288.  Characterization.  This  di.sease  is  characterized 
by  a  high  temperature,  rapid  course,  jaundice  and  anemia. 
These  are  due  to  the  invasion  of  the  blood  with  Piroplas77ia 
ca?iis. 

§  289.  History.  In  1895,  Plana  and  Galli-Valerio 
found  the  piroplasma  in  the  blood  of  dogs.  In  1899,  Hutcheon 
described  a  malarial  fever  in  dogs  that  could  be  transmitted  by 
inoculation  subcutaneously  with  the  infected  material.  Koch 
found  the  disease  in  Africa,  and  Celli  mentions  a  modified 
form  of  the  affection  in  Lombardy.  In  1901,  Nocard  and 
Almy  reported  several  cases  of  piroplasmosis  in  dogs  presented 
at  the   clinic    of    the    Alfort    \"eterinarv    School.      Robertson 


ETIOLOGY  373 

described  the  disease  under  the  name  of  malignant  jaundice 
and  pointed  out  its  transmission  by  the  dog  tick  (^Haemaphy- 
salis  leachi).  In  1902,  Nocard  and  Motas  reported  an  experi- 
mental study  of  the  specific  parasite.  More  recently  Nuttall, 
and  Graham-Smith  have  investigated  this  affection. 

^  290.  Geographical  distribution.  This  disease  has 
been  found  in  several  places  in  Africa,  in  Italy  and  in  I{urope. 

§  291.  Etiology.  The  Piroplasma  canis  is  the  cause  of 
this  affection.  Like  Piroplasma  bigernhnun  it  appears  in  two 
forms,  round  and  pear-shaped.  They  nearly  always  occur  in 
the  red  blood  corpuscles.  It  varies  in  its  morphology.  Ac- 
cording to  Marchoux  Piroplasma  canis  in  France  is  larger  than 
Piroplasma  bigeminum  and  single  parasites  occur  more  fre- 
quently. They  vary  in  size  from  2  to  4//.  At  the  beginning 
of  the  disease  usually  single  large  round  forms  appear.  It  is 
said  by  Nocard  and  Motas  not  to  be  pathogenic  for  other 
species  of  animals.  The  parasite  is  said  to  be  transmitted  by 
means  of  certain  insects.  Lounsbur)'  has  demonstrated  that 
Pulex  ser7'a  liceps,  which  is  very  abundant  in  certain  localities, 
plays  a  role  in  its  transmission.  In  Italy  Piroplasma  canis 
is  supposed  to  be  transmitted  by  Ixodes  reduvius.  In  France 
it  is  supposed  to  be  conveyed  by  Dcrmacentor  reticulatiis.  In 
South  xAfrica  it  is  conveyed  by  Haemaphysalis  leachi.  The 
parasite  appears  in  the  blood  in  from  two  to  four  days  after 
artificial  infection. 

Graham-Smith  did  not  find  the  parasites  in  films  from  the 
peripheral  circulation  when  stained  by  Leishman's  method 
until  several  days  after  infection.  The  earliest  day  on  which 
they  appeared  was  the  sixth  day  and  the  latest  the  thirty- 
sixth  day.  In  most  cases  they  were  observed  between  the 
eighth  and  twelfth  days  after  infection.  In  a  few  cases  he 
worked  out  the  percentage  of  red  blood  corpuscles  that  were 
infected.  He  found  that  it  varied  from  .3  to  1.4^0-  ^"ree 
parasites  were  seldom  encountered  in  the  earlier  stages  but 
later  they  became  more  numerous.  The  day  before  death  he 
found  one  free  parasite  to  23  infected  corpuscles,  and  the   day 


374  CANINE    MALARIA 

of  death  the  free  parasites  were  still  more  numerous.  He 
found  little  evidence  of  phagocytosis  in  the  cases  examined. 
Nucleated  red  corpuscles  appeared  in  films  from  three  dogs 
the  day  before  death,  and  in  three  other  dogs  they  appeared 
six  days  before  death.  Blood  pigment  was  present  in  nearlj^ 
all  samples  of  urine. 

The  period  of  incubation  2ii\.Q.x  direct  inoculation  is  about 
three  days. 

?^  292.  Symptoms.  Two  distinct  forms  have  been 
described  :  the  acute  which  is  nearly  always  fatal,  and  the 
chronic  which  often  terminates  in  recovery.  In  the  acute 
form  the  dog  is  dull,  drowsy  and  refuses  food.  It  may  be 
thirsty.  The  temperature  is  high  (io4°F.)  but  after  two  or 
three  days  it  drops  to  subnormal.  Icterus  is  not  constant  and 
the  hemoglobinuria  is  not  always  present.  The  blood  is  pale 
and  it  coagulates  slowly.  The  red  corpuscles  are  reduced  to 
2,000,000  per  cubic  millimeter  or  below.  The  polynuclear 
leucocytes  are  increased  in  number.  Death  nearly  always 
occurs  in  from  three  to  six  days. 

In  the  chronic  cases  the  fever  remains  high  for  from  36  to 
48  hours,  when  it  returns  to  normal.  The  anemia  is  the  most 
constant  sytnptom.  The  mucosae  become  pale  and  the  appetite 
is  poor.  The  symptoms  persist  for  from  three  to  six  weeks. 
Recovery  is  the  rule. 

^  293.  Morbid  anatomy.  The  mucous  membranes  are 
pale  and  the  subcutaneous  tissue  and  fat  more  yellow  than 
normal.  The  spleen  is  3  or  4  times  the  normal  size.  The 
liver  is  engorged  with  blood  which  is  heavily  charged  with 
parasites.  The  gall  bladder  is  distended  with  greenish  bile. 
The  mucosae  of  the  digestive  tract  are  slightly,  if  at  all, 
changed.  The  kidneys  are  congested,  often  sprinkled  with 
petechise  or  ecchymoses.  The  capsule  is  easily  removed. 
The  parasites  are  found  in  the  blood  in  the  early  stages  of  the 
disease.  They  are  more  numerous  in  the  capillaries  than  in 
the  heart  blood. 

The  lungs  are  in  some  cases  edematous.      In  all    young 


MORinD    ANATOMY  375 

animals  one  finds  edema  of  the  lungs  with  blood  stained  muco- 
serous  substance  in  the  trachea  and  bronchioles.  The 
lymphatic  glands  are  rarely  if  ever  altered  in  appearance. 

The  central  nervous  system  presents  nothing  of  note, 
except  a  slight  congestion  of  the  meninges. 

The  histological  study  of  the  lesions  shows  that  the  tissue 
changes  start  from  greatly  engorged  capillaries.  In  these 
vessels  containing  masses  of  blood,  a  large  part  of  the  red  cor- 
puscles contains  the  parasite. 

The  histological  examination  of  the  organs  when  hardened 
in  Miiller's  fluid  shows,  according  to  Graham-Smith,  the  capil- 
laries of  the  alveoli  of  the  lungs  to  be  dilated  and  in  .some 
instances  a  proliferation  of  the  lining  cells  some  of  which  are 
seen  lying  free  in  the  air  cells.  In  other  alveoli  the  process  is 
more  advanced  and  proliferated  cells,  leucocytes,  and  in  some 
cases  red  corpuscles  are  present  in  them.  The  lumen  of  many 
of  the  bronchioles  frequently  contains  desquamated  epithelium, 
leucocytes  and  mucus.  There  is  no  evidence  of  any  increase 
in  the  connective  tissue.  No  pigmentary  or  fatty  changes  were 
observed  in  the  heart  or  skeletal  muscles.  The  liver  showed 
the  most  marked  changes.  The  central  vein  of  the  lobule  and 
the  capillaries  lying  between  the  liver  cells  were  dilated.  The 
protoplasm  of  the  liver  cells  .stains  feebly  but  the  nuclei  take 
the  stain  fairly  well.  The  cells  are  distorted  between  the 
dilated  blood  vessels  and  in  many  cases  almost  destroyed, 
especially  those  in  the  central  zone.  The  vessels  in  the  inter- 
lobular spaces  are  dilated  but  the  bile  ducts  are  normal.  There 
is  no  increase  of  fibrous  tissue  and  the  capsule  is  normal.  The 
capillaries  contain  a  large  number  of  red  blood  corpuscles  and 
the  proportion  of  leucocytes  is  high.  The  latter  are  also  very 
numerous  in  the  larger  vessels.  In  these  vessels  about  10% 
of  the  red  corpuscles  are  infected.  The  parasites  usually  appear 
in  small  groups  in  the  cells.  The  proportion  of  leucocytes  to 
red  corpuscles  is  about  i  to  10.  In  the  capillaries  from  23  to 
53%  of  the  red  corpuscles  are  infected  and  in  some  instances 
the  proportion  of  leucocytes  to  red  corpuscles  is  as  high  as  r 
to  3.      In  but  one  dog  did  he  find  fatty   changes.     The   smear 


376  CANINE    MALARIA 

preparations  showed  that  gS.g%  of  all  infected  corpuscles  con- 
tained one  to  four  parasites  and  the  balance  more  than  four 
parasites.  Free  parasites  were  found  in  the  proportion  of  i  to 
2}4  infected  corpuscles.  The  spleen  pulp  contains  in  most  cases 
a  large  quantity  of  blood  and  the  vessesl  in  the  trabeculae  are 
dilated  and  contain  numerous  leucocytes.  The  proportion  of 
infected  corpuscles  in  the  pulp  is  small  (3  to  12%)  but  in  the 
small  trabecular  veins  it  is  high  (48%).  In  the  kidney  there 
were  no  changes  that  were  constantly  present  except  dilatation 
of  the  blood  vessels.  In  some  cases  about  46%  of  the  red 
corpuscles  in  the  vessels  of  the  glomeruli  were  infected. 
T/ie  duration  in  fatal  cases  is  from  3  to  6  days. 

§  294.      Differential  diagnosis.     The  positive  diagnosis 
is  made  by  finding   the   parasite  in  the   red   blood   corpuscles. 

REFERENCES 

1.  Graham-Smith.     Canine    piroplasmosis.      Morbid    .\natomy. 
Jour,  of  Hygiene,  Vol.  V  (1905I,  p.  250. 

2.  HuTCHEON.     Malignant  malarial  fever  of  the  dog.      The   Veter- 
inary Journal,  Vol.  XLIX  (1899),  p.  398. 

3.  LouNSBURV.     Transmission  of  malignant   jaundice.     Agricul 
tiiral  Journal,  Nov.  21,  1901. 

4.  Marchoux.      Piroplasma   canis   chez   les   chiens  du   vSenegal. 
Cotnp.  R.  de  la  Societe  de  biologie,  1900,  p.  97. 

5.  NoCARD  ET  AI.MV.     Une  observation   de   piropiasmose    canine. 
Bulletin  de  la  Societe  cent,  denied.  Viler.,  1901,  p.  192. 

6.  NocARD  ET  MoTAS.     Contribution  a  I'etude  de  la  piropiasmose 
canine.     Arm.  de  f  Inst.  Pasteur,  1902,  p.  257. 

7.  Nlittall  AND  Graham-SmiTh.     Canine  piroplasmosis.    Jour, 
of  Hygiene,  Vol.  V  (1905),  p.  237. 

8.  NuTTAi,!..     Canine  piroplasmosis.    Jour,  of  Hygiene,    \o\.    IV 
(1904),  p.  219. 

9.  PiANA  ET  Galli-Valerio.  //  iHodemo  Zooiatro.   1895,  p.  165. 
ID.     Robertson.     Malignant  jaundice  in   the  dog.      77/.?  four,    of 

Comp.  Path,  and  Thera.,  Vol.  XI\'  (1901),  p.  327. 

11.  Webb.     Piroplasmosis  in  Fox-hounds  in  India.       The  four  of 
Comp.  Path,  and  Thera.,  Vol.  XIX  (1906],  p.  i. 

12.  Wetzi..     Ueber  die  Piropiasmose  der  Hunde.     Zeitschrift  fur 
Thiermed.,  Bd.  X,     S.  369. 

13.  Wright.     Canine  piroplasmosis    (on   certain   changes   in   the 
blood),    four,  of  Hygiene,  Vol.  V  (1905),  P-  268. 


CHAPTER  X. 

DISEASES  CAUSED  BY  PROTOZOA 
GENUS  AMEBA. 


§  295.  General  discussion  of  Ameba.  The  ameba 
belong  to  the  class  Sarcodina.  They  include  the  simpler 
forms  of  the  protozoa.  The  genus  ameba  is  provided  with 
lobar  or  pointed  pseudopodia.  A  few  of  these  have  become 
parasitic.  So  far  as  seems  to  be  known,  these  parasites,  with 
possibly  a  few  exceptions,  do  not  produce  noxious  products 
like  bacterial  toxines  or  ptomaines,  but  whatever  damage  they 
may  cause  is  due  to  the  mechanical  disturbances  set  up  by 
their  presence  and  multiplication.  The  genus  ameba  has 
very  few  pathogenic  species.  The  best  known  of  them  is 
Avieba  coli,  the  supposed  cause  of  a  form  of  dysentery  in  man. 
In  animals  but  few  species  have  been  found  to  stand  in  a 
causal  relation  to  a  morbid  process.  The  term  ''amebiasis" 
has  been  introduced  by  Musgrave  and  Clegg  to  denote  an  in- 
fection with  ameba. 


INFECTIOUS  ENTRRO-HEPATITIS  IN  TURKEYS. 
Synonym.     Blackhead. 

§  296,  Characterization.  This  disease  of  turkeys  is 
characterized  by  thickening  of  areas  or  of  the  entire  walls  of 
the  ceca  and  areas  of  tissue  degeneration  and  necrosis  in  the 
liver. 

J^  297.  History.  In  the  fall  of  1893,  Prof.  Samuel 
Cushman  of  the  Rhode  Island  State  Experiment  Station  sent 
a  few  specimens  of  the  affected  organs  of  turkeys  which  had 
died  of  "blackhead"  to  the  Bureau  of  Animal  Industry,  where 


378  ENTERO-HEPATITIS    IN    TURKEYS 

they  were  carefully  examined  by  Dr.  Theobald  Smith.  In  the 
summer  of  1894,  Smith  made  a  careful  study  of  this  disease  at 
the  Rhode  Island  Experiment  Station.  He  found  that  it  was 
caused  by  one  of  the  protozoa  {A^neba  meleagridis.  Smith). 
He  published  a  full  description  of  the  disease  which,  in  accord- 
ance with  the  lesions,  he  designated  Infectious  entero-hcpatitis . 

In  1895,  the  disease  was  further  investigated  respecting 
the  mode  of  transmission  of  the  infecting  protozoa.  The 
results  showed  that  it  could  be  transmitted  directly  from  dis- 
eased to  healthy  turkeys  without  the  intervention  of  an  inter- 
mediate host.  These  results  were  published  in  1896.  The 
place  and  the  time  of  the  first  appearance  of  this  disease  are 
not  clearly  stated,  but  it  seems  that  New  England  was  the  first 
to  suffer  from  it. 

Recently,  Chester  of  the  Delaware  Agricultural  Experi- 
ment Station  has  shown  that  a  very  similar  disease  attacks 
chickens. 

§  298.  Geographical  distribution.  The  available  data 
bearing  upon  the  geographical  distribution  of  this  disease  in- 
dicate that  it  is  widely  distributed.  The  New  England  states, 
particularly  Rhode  Island  and  certain  districts  in  the  Middle 
and  Western  states,  are  affected.  It  has  not  yet  been  reported 
from  the  Southern  states.  For  want  of  statistics  the  amount 
of  loss  to  the  poultry  industry  occasioned  by  this  disease  can 
not  be  accurately  estimated,  but  the  fact  that  it  has  caused 
many  farmers  and  poultry  men  in  New  England  to  discontinue 
the  raising  of  turkeys  shows  that  it  is  of  much  economic  im- 
portance. It  is  stated  in  the  report  of  the  Rhode  Island  Ex- 
periment Station  for  1894  that  "the  eradication  of  this  disease 
would  be  worth  hundreds  of  thousands  of  dollars  to  the  east- 
ern farmers  alone."  These  heavy  losses  in  the  East,  together 
with  the  accumulating  evidence  that  the  entire  northern  third 
of  this  country  is  sprinkled  with  infected  districts  from  which 
the  disease  is  spreading,  indicate  that  this  malady  is  of  more 
than  ordinary  significance  to  those  engaged  in  the  turkey 
industry. 


KTIOLOCiY 


379 


>^  299.  Etiology.  In  1895,  Smith  described  a  micro- 
organism belonging  to  the  protozoa  which  lie  found  to  be 
associated  directlj'  with  the  disease  process.  He  designated 
it  Amicba  rneleagridis.  In  those  cases  in  which  the  disease  was 
recent,  or  at  its  height,  the  parasites  were  very  numerous  in 
the  affected  tissues,  while  in  those  in  which  the  disease  pro- 
cess was  far  advanced  and  associated  with  degenerative  or 
regenerative  changes,  the  parasites  were  found  with  difficulty. 
Curtice  finds  that  the  chicken  is  a  host  for  the  causative  para- 
sites, and  together  with  the  adult  turkeys  spreads  them  broad- 
cast through  the  droppings.  He  has  shown  that  the  ameba 
are  not  transmitted  through  the  eggs.  The  young  turkeys 
become  infected  soon  after  being  exposed  to  contaminated 
surroundings.  The  young  are  much  more  susceptible  than 
the  older  turkeys. 

The  most  fre- 
quent appearance  pre- 
sented by  the  para- 
sites is  that  of  round 
homogeneous  bodies 
with  a  sharply  de- 
fined, si  n  g  1  e  -  CO  n  - 
toured  outline.  With- 
in these  bodies  and 
situated  somewhat 
eccentrically  is  a 
group  of  very  minute 
granules,  probably 
representing  a  nuclear 
structure.  They  vary 
somewhat  in  size, 
measuring  from  8  to 
10  /<  in  diameter  in 
some  cases,  from  12  to  14//  in  others.  In  the  fresh  ti.ssues 
they  are  distinctly  larger  than  the  parasites  within  the  tissues 
which  have  undergone  the  hardening  process.  The  latter  are 
from  6  to  10  //  in  diameter.     The    difference    may    be    due    to 


■scji"--^" 


5^ 


Fig  98.  Ameba  rneleagridis.  (/)  Isolated 
organisms,  (i-)  single  parasites,  (j  1  groups  of 
the  parasite  (a)  of  the  ameba  in  the  mucous 
Diembrane  of  a  turkey'' s  cecum  {Smith). 


38o  EXTERO-HEPATITIS    IN    TURKEYS 

shrinkage,  on  the  one  hand,  and  on  the  other  to  a  sliglit  flat- 
tening of  the  bodies  by  pressure  in  the  fresh  preparations. 
These  peculiar  homogeneous  bodies  were  found,  as  a  rule,  free 
in  the  crushed  preparations,  although  occasionally  giant  cells 
were  detected  which  contained  a  number  of  them.  The  cell 
nuclei  of  the  giant  cells  are  not  visible  in  the  fresh  condition. 
Numerous  coarse  granules,  less  frequently  fat  globules,  are 
embedded  in  its  protoplasm. 

Smith  believed  from  the  results  of  his  investigations  that 
the  parasite  lived  in  the  interstices  and  lymph  spaces  of  the 
tissue,  but  not  within  cells.  This  seems  certainly  true  of  the 
cecum.  The  liver  cells  become  necrotic  or  else  disappear  so 
rapidly  that  it  is  impossible  to  determine  just  where  the  para- 
sites begin  to  multiply.  They  do  not  live  within  the  blood 
vessels,  as  they  are  not  found  within  them  excepting  perhaps 
in  a  thrombosed  vessel.  They  must,  therefore,  occupy  the 
place  of  the  liver  cells.  It  is  probable  that  they  begin  to 
multiply  in  the  connective  tissue  adjoining  the  blood  vessel 
and  simply  crowed  out  the  liver  cells,  leaving  the  connective 
tissue  stroma  of  the  lobules  in  whose  meshes  they  are  found. 

Their  presence  within  giant  cells  is  seen  in  almo.st  every 
infected  organ  subjected  to  examination.  In  teased  prepara- 
tions the  fresh  tissues  they  are  frequenth-  found  with  remnants 
of  the  inclosing  cells  still  attached.  This  intracellular  condi- 
tion is,  however,  a  purely  passive  one  so  far  as  the  parasite  is 
concerned. 

The  microparasites  within  the  tissue  of  the  host  seem  to 
tend  toward  destruction.  Both  the  death  of  the  tissue  itself 
and  the  repair  seem  to  lead  to  the  disappearance  of  the  para- 
sites. In  most  cases  there  may  be  seen  in  the  same  section  a 
partial  dissolution  of  some  of  the  bodies,  while  others  are  still 
in  good  preservation.  Evidently  their  life  within  the  tissues 
is  not  very  long. 

A  discharge  of  the  microparasites  which  escape  destruc- 
tion probably  takes  place  from  the  walls  of  the  ceca,  when 
these  break  down  into  the  contents  with  which  they  are  carried 
outward.      A  similar   discharge  may  take  place  from  the  liver 


ETIOLOGY  381 

through  the  bile  ducts  into  the  intestine.  Another  way  of 
dissemination  is  in  the  death  of  the  diseased  turkey  and  the 
dissolution  of  its  body,  whereby  the  organisms  are  set  free. 

The  occurrence  of  amebre  in  intestinal  affections  of  man 
was  noticed  by  Losch  in  1875.  Since  that  time  it  has  been  the 
subject  of  many  investigations. 

The  points  of  analogy  between  the  avian  and  the  human 
disease  are  that  in  both  there  is  an  affection  of  the  intestine 
(large  intestine  in  man,  ceca  in  turkeys)  associated  with  liver 
disease  due  to  amebae. 

The  intestinal  wall  in  amebic  dysentery  is  greatly  thick- 
ened, owing  to  an  edematous  condition.  It  is  also  thickened 
in  circumscribed  areas  and  contains  cavities  filled  with  gela- 
tinous-looking pus.  The  aniebae  vary  much  in  size  and  con- 
tain vacuoles.  They  are  found  in  variable  numbers  in  the 
bottom  of  the  ulcers  and  in  the  discharges.  The  large  num- 
bers of  amebse  found  in  the  intestinal  contents  led  Councilman 
and  Lafleur  to  infer  an  active  multiplication  therein.  The 
presence  of  the  parasites  within  the  submucosa  is  described  by 
these  authors  in  one  case  only. 

In  the  turkey,  the  parasites  are  always  present  in  the 
connective  tissue  spaces  of  the  mucous  and  submucous  mem- 
brane. Their  presence  in  the  contents  of  the  cecum  is  highly 
probable. 

It  differs  from  the  Ameba  dysenteri<c  in  being  quite  uni- 
form in  appearance,  varying  but  .slightly  in  size  (from  6  to 
io/<  in  diameter)  and  in  being  free  from  vacuoles.  Move- 
ments characterized  as  ameboid  have  not  yet  been  demon- 
strated. 

The  liver  affection  in  man  appears  usually  as  an  abscess. 
In  turkeys  it  appears  as  a  variable  number  of  foci  in  which 
the  microparasites  may  be  present  in  great  abundance.  The 
difference  in  the  nature  of  the  lesions  must  be  largely  attri- 
buted to  the  different  reaction  of  the  tissues  of  birds  toward 
injuries. 

§  300.  Symptoms.  Diarrhea  is  the  symptom  which 
sooner  or  later  may  be  expected  to  appear.      It  probably  occu- 


382  ENTERO-HEPATITIS    IN    TURKEYS 

pies  the  most  prominent  place  among  the  objective  manifesta- 
tions. The  disease  of  the  ceca  is  presumably  responsible  for 
this.  Diarrhea  occurs  with  at  least  one  other  disease  of  the 
ceca  and  with  the  presence  of  tapeworms.  Emaciation  is  pro- 
nounced in  very  chronic  cases  but  it  is  not  constantly  present. 
As  it  may  accompany  other  wasting  diseases,  it  can  not  be  de- 
pended upon  as  an  indication  of  this  affection.  As  the  disease 
progresses  the  turkeys  become  less  active,  lag  behind  their 
flock  or  do  not  go  out  with  it.  Later  the  comb,  wattles  and 
even  the  skin  of  the  head  become  dark  colored,  hence  the 
popular  name  "blackhead."" 

§  301.  Morbid  anatomy.  Turkeys  are  attacked  quite 
young.  Smith  found  a  turkey  about  three  weeks  old  in  which 
the  disease  had  already  made  considerable  progress.  It  seems, 
moreover,  as  if  the  disease  is  contracted  only  by  the  young, 
because  in  the  examination  of  turkeys  of  different  ages  the 
oldest  show  lesions  of  the  longest  standing  ;  that  is,  such  as 
had  undergone  the  most  extensive  transformation.  In  general 
it  may  be  said  that  the  age  of  the  turkey  corresponds  with  the 
age  of  the  disease  process.  The  most  serious  and  extensive 
destruction  of  tissue  occurs  in  the  turkeys  in  the  fall.  In  raid- 
summer  the  disease  is  making  most  progress  and  the  micro- 
parasites  are  present  in  greater  numbers.  It  is  probable  that 
the  delicate  tissues  of  the  3'oung  are  best  adapted  for  the  tem- 
porary habitat  and  rapid  multiplication  of  this  parasite. * 

The  primary  seat  of  the  disease  is  the  ceca.  From  these 
the  liver  is  secondarily  invaded.  Other  organs  have  not  been 
found  to  be  attacked. 

The  lesions  of  the  ceca  are  in  substance  a  thickening  of 
the  wall,  followed  in  most  cases  by  a  destruction  of  the 
epithelium  and  deeper  portions  of  the  mucous  membrane. 
This  destruction  results  in  the  outpouring  of  a  coagulable 
fluid  into  the  tube.  The  thickening  of  the  wall  may  vary 
considerably  in  extent  from  case  to  case. 

*Iii  this  regard  it  simply  follows  the  rule  observed  by  large  numbers 
of  parasites  whose  most  destructive  action  is  visited  upon  the  young. 


.MOKHin    ANATOMY 


383 


It  may  be  uniform  over  the  greater  portion  of  the  tube  or 
it  may  be  limited  to  circumscribed  patches.  The  commonest 
seat  of  these  lesions  is  near  the  blind  end  of  the  tube  where  it 
evidently  starts  and  whence  it  spreads  to  other  portions.  Not 
infrequently  only  one  cecum  is  dis- 
eased, the  other  remaining  normal. 

The  affection  of  the  cecum  is  due 
primaril}^  to  the  multiplication  of  the 
microorganism  which  may  take  place 
chiefly  either  in  the  mucous  mem- 
brane, or  iu  the  submucous  tissue;  it 
may,  though  rarely;  extend  into  the 
muscular  coat.  The  thickening  of 
the  wall  is  the  result  of  several 
processes— the  multiplication  of  the 
parasites,  the  increase  of  the  normal 
tissue  elements  and  later  on  the  ac- 
cumulation of  masses  of  small  cells 
and  some  giant  cells. 

In  the  early  stages  of  the  inva- 
sion, the  adenoid  tissue  between  the 
tubules  and  in  the  submucosa  becomes 
greatly  increased,  owing  to  the  pres- 
ence of  large  numbers  of  micro- para- 
sites of  round  or  slightly  oval  outline 
and  from  6  to  lo/i  in  diameter  which 
stimulates  the  proliferation  of  the  tis- 
sue cells.  Numerous  mitoses  have 
been  seen  in  this  stage.  The  parasites 
seem  to  occupy  the  meshes  of  the 
adenoid  tissue  either  singly  or  in 
groups  or  nests.  In  these  meshes 
they  are  soon  inclosed  in  cells  acting 
as  phagocytes,  so  that  the  appearance 

of    an    intracellular    habitat   of    the   parasites    is   suggested. 

The  presence  of  the  parasites  in  this  reticulum  probably 

stimulates   also   the   accumulation  of   lymph   cells  within   the 


Fig.  99.   Ceca  of  a  turkey; 
[a)   and  {h)   are  diseased 
areas,  {c)  a  section  of  the 
thick  en  ed  wall. 


384 


ENTERO-HEPATITIS    IX    TURKEYvS 


spaces,  by  virtue  of  which  the  mucous  membrane  is  thickened. 
In  this  early  stage  of  invasion  the  epithehum,  both  of  the 
tubules  and  of  the  surface,  remains 
unaffected.  The  parasites  do  not 
invade  the  epithelium  at  any  time. 
As  the  disease  progresses  there 
is  a  continued  increase  in  cellular 
elements  of  the  mucous  and  sub- 
mucous coats  and  a  gradual  inva- 
sion of  the  muscular  coat.  Here 
the  bundles  of  fibers  of  the  circular 
coat  are  thrust  apart  by  masses  of 
cells,  so  that  this  coat  also  becomes 
greatly  thickened.  The  inflamma- 
tion finally  extends  to  the  serous 
covering,  where  the  blood  vessels 
become  greatly  dilated  and  give  the 
cecum  a  congested  appearance.  In 
cases  of  ordinary  severity  the  wall 
of  the  cecum  which  is  not  more 
than  0.2  to  0.5  mm.  thick  normalh' 
becomes  2  to  3  mm.  thick. 

With  the  progress  of  the  dis- 
ease the  mucous  membrane  may  be 
shed  and  a  coagulable  fluid  poured 
out  into  the  cecum.  In  some  cases 
it  appears  in  isolated  masses,  which 
adhere  to  certain  spots  of  the  mu- 
cous membrane.  In  others,  this 
exudate  fills  the  entire  tube  with  a 
yellowish-white  mass,  built  up  in 
concentric  layers  consisting  of  a 
mixture  of  blood  corpuscles,  fibrin 
and  small  round  cells  in  variable 
proportion. 

In  the  further  progress  of  the  local  disease  it  is  not  im- 
probable that  bacteria  are  also  concerned.     The  exudate  con- 


FiG.    100       Diseased  cecum, 

shoziiing    thickness    of   zvall 

and  ulcerated  tnncosa. 


MORBID    AXATOMV 


38; 


tains  immense  numbers  of  them  and  the  denuded  mucosa  fur- 
nishes a  favorable  place  of  entr>-.  It  is  otherwise  difficult  to 
explain  the  continued  increase  in  tliickness  of  the  walls  of  the 
cecum  after  the  mucous  membrane  has  been  shed.  This  con- 
tinued increase  in  thickness  is  due  to  an  extensive  infiltration 
of  small  round  cells  and  the  presence  of  some  giant  cells. 
Parasites  in  this  advanced  stage  are  scarce  and  usually  recog- 
nizable only  as  vacuole-like  bodies  within  the  giant  cells. 

The  thickening  of  the  wall  is  associated  in  some  cases 
with  an  extension  of 
the  inflammation  to 
the  contiguous  wall  of 
the  intestine,  which 
becomes  firml}^  at- 
tached to  the  cecum. 
Yellowish  exudates 
are  sometimes  found 
outside  of  the  diseased 
cecum  on  its  serous 
covering  and  they 
bind  it  inextricably 
to  the  other  cecum  or 
to  the  intestine  or  at- 
tach it  to  the  abdom- 
inal wall.  In  these 
stages,  the  micropara- 
site  is  not  found.  It  seems  to  have  done  its  work  by  destroy- 
ing the  mucous  membrane  and  to  have  left  the  field  for 
miscellaneous  bacteria. 

Other  portions  of  the  digestive  tract  are  not  affected. 
The  secondary  lesions  are  found  in  the  liver,  although  in  some 
cases  they  do  not  appear.  The  organ  itself  is  enlarged  to 
probably  twice  the  normal  size.  Over  the  surface  are  distrib- 
uted roundish,  discolored  spots,  distinctly  demarcated  from 
the  surrounding  tissue.  These  may  be  distributed  uniformly 
over  the  whole  surface  of  the  liver  or  they  may  be  limited  in 
number  to   a  few.     They  vary  from  3  to  15  mm.  in  diameter. 


Fig.  ioi.     Liver  slu 


diseased  foci. 


386 


ENTERO-HEPATITIS    IN    TURKEYS 


Several  types  of  these  spots  appear  corresponding  to  different 
conditions  of  the  diseased  tissue.  We  have  in  the  early,  most 
active  disease  process  sharply  defined  circular  areas  of  a  lemon 
yellow,  or  a  neutral  gray  or  of  an  ochre  yellow  color.  The 
spot  is  not  homogeneous  in  structure,  but  made  up  of  a  deli- 
cate network  of  gi^yish  yellow,  dead  tissue. 

In  another  class  of  spots  there  is  a  mottled  brownish  color 
which  contrasts  only  slightly  with  the  surrounding  liver  tissue 
by  its  darker  color.  It  may  contain  a  central  yellow  nucleus 
of  dead  tissue  and  a  narrow  outer  border  of  the  same  character, 
or  the  border  may  be  a  dark  brownish  circular  line.  The 
entire  spot  has  an  indistinct  appearance  and  is   flattened   or 

even  slightly  depressed 
below  the  surface.  In 
some  cases  they  are 
uniformly  whitish  and 
shade  off  somewhat 
gradually  into  the  sur- 
rounding tissue.  In 
sections  of  the  affected 
organ  it  will  be  found 
that  the  surface  spots 
represent  masses  of 
liver  tissue  in  the  same 
condition,  the  spots  be- 
ing simply  the  places 
where  these  diseased 
foci  intersect  the  sur- 
face. Some  are  found 
deeply  imbedded  in  the 
liver  tissue,  and  therefore  not  visible  on  the  surface.  The 
lesion  of  the  liver  is  thus  represented  by  few  or  many  foci  of 
disease  having  in  general  a  spherical  form  and  appearing  on 
the  surface  of  the  organ  as  round  spots.  Occasionally  the 
lesions  become  more  extensive  and  the  death  of  large  portions 
of  liver  tissue  follows. 

The  changes  in   the   liver   are   most  easily  explained  by 


r^' 

-  ■'  - 

1 

'.  ^    ''^: 
^^" 

^' 

Fig.  I02.  A  drait'iiig  of  a  beginning  ne- 
crotic mass,  (a)  Giant  cells,  {€)  free  nuclei, 
and  [b)  disintegrated  necrotic  tissue. 


MORI5ID     ANATOMY  387 

assuming  that  the  niicroparasites  are  convej-ed  by  the  blood 
directh'  from  the  diseased  ceca  into  the  liver  and  there  de- 
posited in  different  places,  where  they  begin  to  multiply  and 
spread  in  all  directions.  In  this  way  they  form  the  spherical 
foci  of  disease  which  appear  as  circles  on  the  surface  of  the 
liver.  This  theory  is  borne  out  by  the  results  of  the  micro- 
scopic examination. 

In  sections  of  hardened  tissue  from  the  liver  in  which  the 
disease  has  but  recenth^  begun,  the  affected  regions  are  invaded 
b}^  large  numbers  of  protozoa  which  occupy  a  kind  of  reticu- 
lum formed  probably  from  the  connective  tissue  stroma.  The 
liver  cells  have  partially  or  wholly  disappeared  from  these  foci. 
The  border  of  the  necrotic  tissue  is  surrounded  bj'  a  zone  of 
giant  cells.  The  parasites  occupy  the  meshes  of  the  tissue 
either  singly  or  in  groups.  The  reticulum  is  provided  with  a 
small  number  of  nuclei,  some  of  which  are  closely  applied  to 
and  curved  partly  around  the  parasite.  The  blood  vessels  are 
usually  much  dilated  and  filled  with  red  corpuscles. 

The  yellow  masses  observed  with  the  naked  eye  in  the 
surface  spots  are  shown  to  be  patches  of  an  amorphous  sub- 
stance which  take  nuclear  stains  very  feebly,  the  aniline  colors 
not  at  all.  This  may  be  described  as  a  coarse  network  in  the 
meshes  of  which  small  cells,  and  very  rarely  parasites,  are 
seen.  This  substance  is  assumed  to  be  the  result  of  coagula- 
tion necrosis  of  the  liver  cells  by  which  they  have  lost  their 
nuclei  and  have  become  fused  into  a  formless  mass.  It  is 
probable  that  the  plugging  of  blood  vessels  in  the  liver  by 
parasites  carried  from  the  cecum  is  the  cause  of  the  necrosis, 
since  such  plugs  or  thrombi  are  not  uncommon  in  sections  of 
the  diseased  areas. 

With  the  appearance  of  the  niicroparasites  regenerative 
changes  begin  at  once  which  complicate  the  process.  We 
have  at  the  outset  an  active  multiplication  of  the  niicropara- 
sites which  take  the  place  of  the  original  liver  tissue  and  a 
process  of  coagulation  necrosis  going  on  at  the  same  time. 
Soon  multinucleated  (giant)  cells  appear.  Not  infrequently 
they    are    grouped    around    what    appears    to    be  a  plugged 


388  ENTERO-HEPATITIS    IX    TURKEYS 

vessel    or    else    they    occupy    the    lumen  of    the  vessel   itself. 

In  still  older  cases  the  diseased  areas  are  found  more  or 
less  filled  with  small  round  cells  which  may  have  passed  into 
the  dead  regions  from  the  blood  vessels.  In  all  cases  the 
latter  are  more  or  less  enlarged  and  they  seem  to  encroach 
upon  the  liver  tissue,  thus  filling  in  part  the  void  produced  by 
the  cell  death  and  giving  the  surface  of  the  liver  a  brownish, 
mottled  appearance  wherever  the  disease  spots  are.  The 
proce.sses  of  advancing  disease  and  necrosis  or  death  of  tissue 
on  the  one  hand  and  of  repair  on  the  other  seem  to  go  on  side 
by  side,  now  one,  now  the  other,  predominating. 

The  results  of  the  investigations  thus  far  made  indicate 
that  the  disease  may  follow  several  courses. 

1.  After  a  certain  period  of  disease,  regenerative  pro- 
cesses begin  which  tend  toward  a  permanent  recover5\ 

2.  The  disease  may  proceed  so  rapidly  from  the  very 
start  that  the  affected  turkeys  die  early  in  life. 

3.  The  disease  may  come  to  a  standstill  but  the  amount 
of  dead  tissue  in  the  ceca  and  liver  maj'  be  so  great  as  to  favor 
the  entrance  of  bacteria  which  are  directly  responsible  for  the 
death  of  the  bird  late  in  the  summer  or  fall. 

The  description  of  the  lesions  of  a  turkey  dead  of  this 
disease  is  appended.     It  is  quoted  from  Smith's  report. 

"  Turkey  No.  14. — About  5  months  old.  Taken  from  a  flock  August 
8  because  of  lack  of  strength  to  keep  up  with  the  rest  when  driven. 
Indications  of  diarrhoea.  Placed  in  a  coop,  where  it  died  during  the 
night.     Examined  next  morning. 

"Slight  odor  of  decomposition.  A  few  small  warts  on  skin  of  neck. 
The  various  organs  were  found  normal,  with  the   following   exceptions  : 

"Mucosa  of  duodenum  almost  blackish,  from  intense  injection  and 
pigmentation  of  villi. 

"Both  caeca  diseased.  The  left  is  slightly  distended.  On  serous 
aspect  two  yellowish  spots,  with  markedly  injected  borders,  correspond- 
ing to  thickenings  of  the  walls  near  the  blind  end  of  tube.  The  mucous 
surface  of  one  is  smooth  ;  to  the  other  an  exudate  is  attached.  Besides 
the  thickening  of  these  spots,  the  free  half  of  this  caecum  is  somewhat 
thickened  uniformly. 

"The  right  caecum  is  very  much  distended  over  two-thirds  of  its 
length.     From  the  serous  surface    local    thickenings    are    recognizable. 


DIIFERENTIAL    DIAGNOSIS  389 

which  have  a  yellowish,  mottled  appearance.  The  small  intestine  is 
firmly  attached  to  one  of  these.  The  disease  has,  however,  not  invaded 
the  wall  of  the  latter.  The  border  of  these  spots  is  intensely  hypenemic. 
When  the  caecum  is  slit  open  its  width  is  three  to  four  times  that  of  the 
undisturbed  tube,  and  the  thickness  of  the  wall  varies  from  one-eighth 
to  one-half  of  an  inch,  being  not  less  than  one-eighth  of  an  inch  over 
three-fourths  of  the  entire  length.  When  the  brownish  feces  were 
washed  away  the  increased  local  thickenings  were  found  covered  with 
firm  exudates,  usually  attached  in  but  one  spot. 

"Sections  were  examined  of  that  portion  of  the  caecal  walls  which 
was  very  much  thickened,  and  to  which  the  contiguous  small  intestine 
was  inseparably  attached  by  the  new  growth. 

"The  mucosa  of  the  caecal  portion  had  sloughed  away,  while  that  of 
the  embedded  small  intestine  was  intact.  The  neoplastic  tissue  between 
caecum  and  intestine  was  fully  i  cm.  (two-fifths  inch)  thick.  Inas- 
much as  the  infiltration  probably  followed  the  narrow^  mesentery 
between  caecum  and  intestine  the  original  boundary  lines  of  the  caecal 
■wall  are  no  longer  recognizable.  The  muscular  coat  of  the  caecum  may 
be  traced  for  only  a  short  distance  into  the  neoplasm,  when  it  appears. 
Microparasites  were  not  seen  distinctly  in  the  diseased  tissue. 

"The  liver  is  very  much  enlarged,  and  dotted  everywhere  with 
roundish  spots  of  varying  appearance.  The  majority  are  from  5  to  12 
mm.  in  diameter,  round  or  slightly  oval.  The  center  of  each  is  usually 
occupied  by  a  group  of  yellowish  dots  and  the  circle  is  bounded  by  a 
narrow  yellowish  ring.  The  space  of  the  circle  is  mottled  brownish. 
Among  these  spots  there  are  also  circles  of  a  completely  yellowish  color. 
On  the  convex  surface  of  the  left  lobe  there  is  a  very  firm,  ring-like, 
yellowish  mass,  cutting  like  firm  cheese. 

"In  crushed  preparations  of  fresh  liver  tissue  from  within  the  brown- 
ish circles  many  giant  cells  are  seen.  They  consist  of  a  meshwork  of 
protoplasm  of  a  rather  coarsely  granular  character  inclosing  spheres 
which  appear  homogeneous.     The  giant  cells  are  up  to  30  /<  in  diameter. 

"Sections  of  liver  tissue  hardened  in  alcohol  and  in  Foa's  solution 
were  also  examined.  The  foci  of  disease  contain  necrotic  areas  in 
which  are  numerous  giant  cells  each  inclosing  a  number  of  micro-para- 
sites. In  some  portions  there  is  much  cell  infiltration  in  the  interlobu- 
lar tissue  around  the  portal  vessels.  Among  the  cells  the  protozoa  are 
recognizable." 

i^  302.  Differential  diagnosis.  This  disease  is  to  be 
dilTerentiated  from  certain  local  affections  of  the  cecum  not 
especially  uncommon  in  turkeys.  Ztirn  {Deu/sc/ie  Zeit.  /. 
T/iiermed,  Bd.  A' (1883),  p.  189)  has  described  a  cecal  disease 
in  water  fowls  and   turkeys    and    von    Ratz    has  described    a 


390  ENTERO-HEPATITIS    IN    TURKEYS 

cecal  disease  in  turkeys  in  which  the  Hver  lesions  seem  to  be 
absent.  The  lesions  in  the  liver  and  the  presence  of  the 
microparasite,  as  previously  described,  are  sufficient  to 
differentiate  this  disease. 

§  303.  Prevention.  The  present  knowledge  of  this 
disease  .shows  that  the  parasite  is  transmitted  directly  from 
diseased  to  healthy  turkeys.  This  suggests  that  the  first  pre- 
caution is  to  avoid  the  entrance  of  diseased  or  seemingly 
healthy  turkeys  from  a  diseased  flock  into  a  healthy  one. 
The  discovery  of  Chester  indicates  that  a  like  precaution  must 
be  taken  with  reference  to  fowls.  If  the  disease  exists  the 
best,  although  mo.st  radical,  method  as  suggested  by  Smith  is 
the  total  destruction  of  the  affected  flock,  thorough  disinfec- 
tion of  the  roosts  and  droppings  under  the  same,  and  the  intro- 
duction of  healthy  turkeys. 

RKFEREXCES 

1.  Chester.  Report  of  the  bacteriologist  of  the  Del.  College 
Agric.  Kxp.  Station,  1899-1900.     (C.  reports  disease  in  chickens). 

2.  Curtice.  Notes  on  experiments  with  blackhead  of  turkeys. 
Circular  No.  i ig.     Bureau  oj  Animal  Industry,  1907. 

3.  CuSHMAN.  Nature  of  blackhead  in  turkey.  Report  R.  Island 
Agric.  Exp.  Station,  1894,  p.  199. 

4.  MooRE.  The  direct  transmission  of  infectious  entero-hepatitis 
in  turkeys.     Circular  No.  5,  Bureau  of  Animal  Industry,  1896. 

5.  MuSGRAVE  AND  Clegg.  Amebas  :  Their  Cultivation  and  Etio- 
logic  Significance.  Bulletin  No.  18.  Bureau  of  Cover7iinent  Labora- 
tories, Manila,  1904. 

6.  Smith.  Infectious  entero-hepatitis  in  turkeys.  Bulletin  No. 
S,  U.  S.  Bureau  of  Animal  Industry,  1895. 


chapti<:r  XI. 

DISEASES  CAUSED  BY  PROTOZOA 
GENUS  TRYPANOSOMA. 


§304.  Classification  of  Trypanosoma.  The  Trypan- 
osoma belong  to  the  protozoa,  but  their  species  diagnosis  is 
not  satisfactorily  determined.  A  number  of  classifications  of 
these  organisms  have  been  proposed.  The  one  suggested  by 
Salmon  and  Stiles  is  appended. 

Protozoa,  class  Mastioophora,  subclass  Flagellata,  order 
Monadida,  family  Trypanosomidae,  genus  Trypanosoma  Gruby. 

According  to  Stiles  the  family  contains  at  present  two 
genera,  which  are  distinguished  as  follows  : 

1.  One  flagellum  present,  extending  from  the  centrosome  along 

the  undulating  membrane  and  becoming  free  at  the  anterior 
extremity Trypanosoma 

2.  Two      flagella,    one    extending    anteriorly,    the    other    pos- 

teriorly   Try paiio plasma 

Generic  diagnosis  of  Trypanosoma.  "  Body  fusiform,  presenting  a 
lateral,  longitudinal,  undulating  membrane,  the  thickened  border  of 
which  terminates  posteriorly,  in  the  posterior  half  of  the  body  in  a 
'  centrosome,' and  is  prolonged  anteriorly  in  a  free  major  flagellum; 
nucleus  generally  anterior;  there  is  a  tendency  to  agglomeration  by 
the  posterior  extremity  ;  divisions  longitudinal  and  unequal.  Parasitic 
in  the  blood  of  vertebrates." 

In  order  that  a  somewhat  definite  idea  of  the  structure  of 
these  organisms  may  be  obtained  the  specific  characters  of  Tr. 
Lewisi  are  quoted. 

Trypanosoma  :  "  8  to  10  //  long,  2  to  3  //  broad,  24  to  34  n  long  by 
1.44  broad  (Laveran  and  Mesuil.  1901)  ;  a  very  refringent  granule  (near 
centrosome)  in  place  of  which  a  clear  vacuole  is  seen  in  stained  prepara- 
tions. Animalcules  exceedingly  minute,  alternate  and  vermicular 
under  normal  conditions,  but  highly  polymorphic  and  capable  of  assum- 
ing a  variety  of  contours  ;  flagellum  single,  terminal,  two  or  three  times 
the  length  of  the  extended  body.  No  contraclible  vesicle  ...  as 
yet  detected.     Habitat,  blood  of  the  rat  and  hamster." 


392 


TRYPANOSOMA 


§  305.  General  morphology  of  trypanosoma,  Try- 
panosoma of  all  species  are  in  general  very  similar.  The  mor- 
phology is  said  to  vary  greatly  in  the  same  species  and  to  a 
greater  extent  in  different  species.  In  general  the  trypanosoma 
may  be  said  to  measure  from  i  to  5  /i  in  thickness  and  from  15 
to  45  /<  in  length,  including   flagellum.     They   all  show  very 

active  eel-like  movements 
and  some  motility.  The 
nature  and  extent  of  the 
motility  varies.  The  fact 
as  stated,  that  variations 
are  occasionally  found  in 
one  species,  often,  indeed, 
in  a  single  preparation, 
which  are  nearly  as  great  as 
those  observed  between  dif- 
ferent species,  renders  the 
specific  determination  dififi- 
cult.  The  flagellum  at  the 
anterior  end  of  the  parasite 
varies  gre.atly  in  length.  It 
is  actively  motile,  pointed 
and  continuous,  with  the 
thickened  margin  of  the 
undulating  membrane  end- 
ing at  or  near  the  centre- 
some.  The  undulating 
membrane  extends  along 
the  border  of  the  organism 
from  near  the  ceutrosome  in  the  posterior  portion  to  the  anterior 
end  of  the  organism,  from  whence  it  continues  as  the  free 
flagellum.     Its  breadth  and  folds  vary  considerably. 

The  nucleus  is  usualh'  situated  in  the  anterior  half  of  the 
parasite  and  varies  both  in  size  and  shape.  It  is  generally 
oval  or  round,  and  assumes  other  contours  with  the  different 
stages  of  division.  The  centrosomeas  a  rule  is  in  the  posterior 
and  more  blunt  end,  and  it  appears  to  have  an  intimate  associ- 


FiG.  103.  Trypan- 
osoma Briicei :  c, 
centrosome ;  f, 
flagellum  ;  m, un- 
dulating mem- 
brane; n, nucleus. 
X  about  2,000. 
{After  Laveran 
and  Mesnil). 


Fig.  104.  Trypan- 
oplasma  Borrelli  : 
ccentrosome  ;  fa, 
anterior  flagel- 
lu  in ;  fp  ,posterio  r 
flag  ell  u  ni;  m  ,un- 
dulating  mem,- 
hrane;  n,nucleus; 
X  about  1,800. 
{After  Laveran 
and  Mesnil). 


MULTI  PLICATION 


393 


ation  with  the  llaoelhun  and  undulating  membrane.  Its  loca- 
tion has  been  used  as  a  diagnostic  point  in  determining  species. 
The  protoplasm  is  homogeneous  or  granular,  depending 
upon  the  age  of  the  parasite,  its  environment  and,  perhaps  to 
a  certain  degree,  upon  the  species.  Few  or  many  fine  or 
coarser   granules   may    be    found    scattered    throughout     the 

protoplasm. 

Multiplication.     Voges  gives  three  forms  of  multiplication, 
namely,   longitudinal,    transverse   fission,    and   segmentation. 


r  &  9         ^o         n 

Fig  105.     2,  Trypanosoma  Lewisi  completely  developed  ;  n  '^^f'^*^J^^ 

ZroLe     Jindulatin.rnembrane    f,M^^^^^^^^ 

in  process  of  division.      7—  other  forms  of  '''''^''tf   ''"^"f.^- 

LeLi,  //,  flagella    not    stau,ed.     X    al^out    .,000    durm.te,s    ^ntte, 

Laveran  and  Mesnil). 

He  did  not  observe  conjugation.     The  chromatin  divides  into 

frotn  3  to  10  segments,  which  assume  irregular  shapes  and  loca- 

Uons   some  of  which  areoften  found  well  np  ,n  the  flagellum. 


394  TRYPANOSOMA 

The  nucleus  usually  divides  into  equal  parts,  but  may  break 
into  several  segments.  After  the  nuclear  division  the  proto- 
plasm may  assume  various  irregular  forms.  The  young  nuclei 
arrange  themselves  in  groups,  and  the  parasite  twists  and 
splits  by  longitudinal  or  more  often  by  transverse  fission 
(Fig.  104).  The  new  forms  resulting  from  the  division  soon 
assume  the  regular  shape.  Plimmer  and  Bradford  consider 
longitudinal  and  transverse  division  the  more  frequent  modes 
of  reproduction.  They  observed  conjugation,  which  con- 
sisted in  the  fusion  of  the  micronuclei,  followed  by  an  amoeboid 
stage  and  division  by  segmentation.  The  order  of  division 
appears  to  be  (i)  centrosome,  (2)  flagellum,  and  (3)  nucleus 
and  protoplasm.  Other  forms  of  reproduction  have  been 
described  by  Martini,  Laveran  and  Mesnil  and  others.  Invo- 
lution forms  have  been  observed  by  a  number  of  workers. 
Rodet  and  Vallet  state  that  Tr.  Brucci  multiply  principally  in 
the  blood  and  lymph.  There  is  a  difference  of  opinion  con- 
cerning the  agglutination  of  Trypanosoma.  Musgrave  and 
Clegg  state  as  a  result  of  their  researches  that  the  so-called 
phenomenon  of  agglutination  is  of  no  value  from  a  diagnostic 
point  of  view,  and  it  is  too  uncertain,  if  it  is  a  reaction,  to 
serve  as  an  index  of  immunity  or  susceptibility. 

§  306.  Distribution  in  the  body.  It  is  the  opinion  of 
most  students  of  the  Trypanosoma,  that  in  the  infected  animal 
they  are  found  in  all  of  the  body  juices,  and  are  not  present  at 
the  same  time  in  great  numbers  in  one  part,  with  but  few  in 
another.  Animals  having  many  parasites  in  the  blood  when 
killed  show  them  also  in  the  organs  ;  and  if  they  are  not 
demonstrable  in  a  microscopic  examination  of  tlie  one  they  will 
not  appear  in  the  other.  The  blood  of  animals  suffering  from 
the  disease  is  always  infectious  by  animal  inoculation, 
although  the  parasites  may  not  be  found  microscopically  at  the 
time.  Martini,  however,  regards  the  spleen,  lymphatics,  bone 
marrow,  and  to  a  less  extent,  the  liver  and  kidneys,  as  the 
places  for  the  destruction  of  Trypanosoma.  It  has  been  found 
that  Trypanosoma  injected  into  the  peritoneal  cavity  multipl>^ 
considerably  before  they  enter  the  blood. 


HISTORY  395 

Disappearance  after  death.  Trypanosoma  disappear  very 
suddenly  after  the  death  of  the  host.  Within  two  hours  signs 
of  degeneration  begin  ;  the  parasites  shrink,  assume  irregular 
shapes  and  then  disappear.  Motile  forms  are  rarely  found 
after  two  hours. 

Distribution  in  nature.  Trypanosoma  are  not  known  to 
exist  in  nature  outside  of  the  bodies  of  living  animals.  They 
have  been  found  in  the  blood  of  a  large  number  of  species. 
Now  has  found  them  m  the  blood  of  many  birds.  1  hey 
have  been  kept  alive  in  blood  or  salt  .solution  for  a  few  hours. 
Novy  has  succeeded  in  cultivating  them,  /.  e..  getting  them  to 
multiply  on  an  artificial  culture  medium. 

R  .07  Historical  sketch.  There  is  a  voluminous 
Hterature  on  the  trypanosoma  from  which  the  following  brief 
summary  was  taken.  In  1841,  Valentin  discovered  hematozoa 
in  trout  ^Salmo  fario)  and  in  1842,  Glugge  found  them  in  the 
blood  of  frogs.  In  1843,  Gruby  observed  a  flagellate  infusorium 
in  frogs  which  he  named  Tr.  sanguinis.  Gruby  has  generally 
been  credited  with  the  discovery  of  these  forms.  From  1843 
to  1879  the  organisms  were  found  by  many  observers,  not  only 
in  frogs  but  in  birds  as  well. 

In  1870-80  Lewis  described  trypanosoma  found  in  rats  in 
India.  Liter  he  states  that  they  are  identical  with  Tr.  Evansr 
In  1880  G.  Evans  discovered  trypanosoma  in  the  blood 
of  horses  suffering  with  surra,  the  well  known  disease  of 
India  He  proved  their  causal  relation  to  the  affection.  In 
X885  Steele  confirmed  Evans'  work,  and  named  the  parasite 
Spirocheta  Evansi. 

The  work  of  Evans  and  Steele   was   followed  by    many 
interesting  discoveries  of  trypanosoma  especially  in  fish  and  in 

Rouget    described    Trypanosonm    found    in    the 


man. 


In    i: 


in     I5QD,    iVUUgcL    v.^^- .. 

blood  of  a  horse  suffering  from  dourine.  W  asilewskj  .  nd 
Senn  in  ,899,  confirmed  Rougefs  work  and  deternnned  the 
pyogenic  acUon  of  this  parasite  for  the  horse.  I.averan  and 
Mesnil  proposed   the   name    Tr.    ,ougM  for   the   parasrte   of 


396 


TRYPANOSOMA 


dourine.  Doflein  (Jul.v,  1901)  named  it  Tr.  equipeydum, 
which  term  was  adopted  b}-  Salmon  and  Stiles. 

In  1901,  according  to  Voges,  Elmassian  first  differentiated 
the  Trypanosoma  of  Mai  de  Caderas  in  South  America.  Voges 
described  it  the  following  year,  demonstrated  its  pathogenic 
action,  and  named  it  Tr.  eqiiimuu . 

In  1902,  Bruce  and  Laveran  independently  published 
articles  inwhich  thev   credit    Theiler  with  the  discovery  of  a 


Fig.  106.     A  map  shozcing  the  geographical  distribution  of 
Trypanosoma  disease. 

new    Trypanosoma  of   cattle    in    South    Africa.       They    each 
proposed  the  name  Tr.  TheiUri. 

In  1901,  Smith  and  Kinyoun  described  a  parasite  which 
had  been  observed  by  Jobling  in  the  blood  of  a  sick  horse 
in  Manila.  Later  in  the  year  Smith  described  it  as  Tr. 
Evansi. 


§  308.     Trypanosomiasis.     Salmon  and  Stiles  have  in- 
troduced  the  term   Trypanosomiasis  to   describe  an  infection 


TRYPANOSOMIASIS  397 

With  parasites  belonging  to  the  flagellate  family  Trypanoso- 
midac  The  term  is  analogous  to  Teniads  and  Cocc^d^os^s. 
There  are  a  number  of  different  trypanosomiases  now  recog- 
nized, being  caused  by  different  species  of  Trypanosoma. 
Among  these  the  following  may  be  mentioned  : 

1  Surra  A  disease  of  equines,  camels,  elephants  and 
certain    other    animals    in    India,    attributed  to    Trypanosoma 

Evansi. 

2  Nagana,  nvgana  or  Tsetse JJy  disease  of  Africa.  Af- 
fecting cattle,  horses,  mules,  asses,  antelopes,  camels  and 
certain  other  animals.     It  is  attributed  to  Trypanosoma  Brueei. 

.  Do^crine  or  maladie  du  eoit  of  Algiers,  France  and 
Spain  ■  It  attacks  the  horse  and  the  ass  in  particular,  but  may 
be  transmitted  to  certain  other  animals.  It  is  attributed  to 
Trypanosoma  equiperdnm . 

'4  ^a/«^.m«'.m.  of  South  America.  It  affects  horses 
assesTcattle,  hogs  and  certain  other  animals.  It  is  attributed 
to  Trypanosoma  eqitinum. 

.       Rat  trypanosomiasis  attributed  to  Trypanosoma  Uwis, 
By  some  authors  this  parasite  is  alleged  to  be  identical  w.th 
the  horse  surra  organism,  but  it  is  quite  certain  that  rats  may 
Itbo,  a  distinct  s-pecies.     Until  the  results  of  f-ther  mvest,- 
gations  are  recorded  it  is  deemed  best  to  consider  these  as  d,s- 
Sct  infections.     Mttsgrave   and   Clegg   include   that   proof 
sufficient  to  establish  the  individuality  of  the    Trypan  soma 
cans  ng  trypanosomiasis  in  domestic  animals  has  not  5^t  been 
advanced      These  authors  consider  the  trypanosonra  found  .n 
domesticated  animals  in  the  Philippine  Islands  as   Tr.  E.ansi 
It  is  important  to  note  the  observation  of  Musgrave  and 
Cle..-  that  "in  all  the  .forms  of  trypanosonnas.s  the  infection 
see^s.o  involve  particularly  the  genitalia,  the  skin,  and  the 
organs  of  special  sense.     The  skin  symptoms  consis   of   ough- 
e  Jng  of  the  hair,  which  also  falls  out  in  places :  a  thickening 
of  the  epidermis,  often  with  exfoliation,  and  in  some  stages  ol 
the   disease,    various   skin   eruptions.     There  may  be  simple 
ervthema,  and  more  rarely  they  may  assume  the  severer  forms. 


398  TRYPANOSOMA 

as  urticaria,  or  in  extreme  cases  a  distinct  localized  ulceration 
may  occur.  The  scrotum  and  penis  in  the  male  and  the  vulva 
in  the  female  are  often  swollen,  and  ulcerations  of  the  penis  or 
vulva  are  frequent  symptoms  especially  in  dourine.'' 

The  geographical  distribution  of  the  trypanosomiases  is 
shown  in  Fig.  io6. 

The  following  table  of  trypanosoma  compiled  by  Smedley 
gives  the  distribution,  means  of  dissemination  and  the  patho- 
genesis of  the  various  species. 

REFEREXCES. 

1.  DuTTox  AXD  Todd.  First  report  of  the  Trypanosomiasis  Ex- 
pedition to  Setieganibia  (1902).  Thomson  yai(S,afid Jofiiison  Labora- 
tories Report,  \o\.  V. 

2.  LAVERA>r  AXD  Mesxil.  Recherches  morphologiques  et  ex- 
perimentales  sur  le  Trypanosomi  des  rats  (Tr.  Lewisi,  Kent).  Ann. 
de  V Inst.  Pasteur  Vol.  XV  I  1901),  p.  673. 

3.  Laverax  et  Mesxil.  Trypanosonies  et  Trypanosomiases. 
Paris.      1904. 

4.  NovY,  McNeal  and  Hase.  The  Cultivation  of  Tr.  Brucei. 
The  Jour,  of  hi fectious  Diseases,  Vol.  r  (1904),  p.  i. 

5.  Petrie.  Observations  relating  to  the  structure  and  geographi- 
cal distribution  of  certain  trypanosomes.  Jour,  of  Hygiene,  Vol.  V 
(1905),  p.  191. 

6.  RoDET  ET  VAtLET.  Contribution  a  I'etude  des  Trypanoso- 
miases.    Airh.  de  Med.  Exper.,  Vol.  XVIII  (1906),  p.  450. 

7.  Smedley.  The  Cultivation  of  Trypanosomata.  The  Jour,  of 
Hygiene,  Vol.  V  {1905),  p.  24. 

8.  Thiroux.  Recherches  morphologiques  et  experimentales  sur 
Trypanosoma  Paddae.    Ann.  de  P Inst.  Fasteur,  Vol.  XIX  (1905),  p.  65, 


TRYPANOSOMATA 


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400  SURRA 

SURRA 

Synonyms.  Relapsing  fever  of  equines;  pernicious  ane- 
mia of  horses. 

§  309.  Characterization.  Surra  is  an  infectious  dis- 
ease of  solipeds  and  camels  caused  by  a  flagellate  protozoan.  It 
is  determined  by  a  continuous  fever  with  alternate  paroxysms 
and  intermissions,  with  a  general  or  localized  eruption  of  the 
skin,  petechiae  of  the  mucosae  and  more  or  less  subcutaneous 
edema.  There  is  rapid  emaciation  and  great  weakness.  It  is 
usually  fatal.  It  attacks  horses,  asses,  mules,  cattle,  goats, 
dogs,  and  rats.  It  can  be  inoculated  into  other  animals  such 
as  rabbits,  guinea  pigs  and  mice.  From  an  economic  point  of 
view  it  is  reported  to  be  essentially  a  disease  of  horses. 

In  India  cattle  are  said  to  be  infected  with  the  trypan- 
osoma  of  surra  but  they  are  not  appreciably  affected  by  them. 
It  is  reported  that  horses  become  infected  by  insects  that  have 
first  bitten  such  cattle. 

sj  310.  History.  This  disease  appears  to  have  been 
known  for  many  years  to  the  natives  of  the  low  lands  on  both 
sides  of  the  Indus  on  the  northwest  frontier  of  India.  Haig 
appears  to  have  observed  it  in  Persia  in  1876.  In  1880,  Evans 
found  several  cases  of  it  in  the  Dera  Ismael  Khan  county.  He 
was  the  first  to  describe  it  and  attribute  its  cause  to  an  animal 
parasite  which  he  discovered  in  the  blood.  In  1885,  Steel  met 
with  a  disease  among  mules  in  Burma  which  he  regarded  as 
identical  with  Evans'  surra,  and  which  he  believed  to  be  re- 
lapsing fever.  In  1888  there  was  an  outbreak  among  the 
Bombay  Tramway  Company's  horses.  Since  then  surra  has 
become  epizootic  in  Bombay;  Lingard  reports  that  thousands 
of  ponies,  horses,  camels  and  asses  died  from  it  during  the 
rains  of  1893  and  1894.  Its  ravages  in  the  Punjab  and  North- 
west Provinces  during  1895  are  reported  to  be  appalling. 

§  311.  Geographical  distribution.  It  is  a  disease  of 
Asia  and  Africa.  It  is  reported  that  "  the  distribution  of  this 
malady  seems  to  be  entirely  influenced  by  the  physical  aspect 


ETIOLOGY  401 

of  this  country;  being  far  more  prevalent  in  those  parts  where 
floods  and  inundations  occur  than  in  the  higher  and  dryer 
portions"  (Pease).  If  the  identity  of  surra  with  tsetse  fly 
disease  proves  to  be  true,  which  is  still  questioned,  it  has  a 
wide  distribution  in  Central  Africa. 

Surra  does  not  exist  in  the  United  States,  but  because  of 
its  prevalence  and  long  standing  in  the  Philippines  it  is  liable 
to  be  introd-uced  into  this  country.  For  this  reason  its  nature 
.should  be  understood  by  American  veterinarians. 

j^  312.  Etiology.  There  is  little  or  no  doubt  that  surra 
is  due  to  the  presence  in  the  blood  of  a  flagellated  infusorian, 
Tn  'pa  n oso m a  Ei  -a  n  s i . 

"  A  motile  trypanosoma  20  to  30//  in  length  to  i  to  2  //  in  breadth, 
somewhat  blunt  at  the  posterior  end  and  gradually  tapering  at  the 
anterior  end.  The  undulating  membrane  is  well  defined,  beginning  at 
or  near  a  small  body  (centrosome)  in  the  posterior  portion  of  the  para- 
site and  extending  forward  as  a  free  flagellum.  It  is  provided  with  a 
nucleus  and  agranular  protoplasm." 

This  organism  is  invariably  found  during  the  paroxysms 
of  the  disease  in  the  blood  of  animals  which  have  acquired 
surra  either  naturally  or  experimentally.  Although  blood 
containing  these  infusoria  readily  communicates  the  disease  to 
susceptible  animals  it  entirely  loses  its  virulence  when  it  is 
filtered  through  porcelain,  so  as  to  free  it  from  the  parasite. 
The  disease  can  be  transmitted  to  healthy,  susceptible  animals 
even  of  different  species  with  the  unfiltered  blood  of  a  diseased 
animal.  The  microscope  reveals  the  infusoria  in  vast  numbers 
moving  with  great  activity  in  the  blood.  When  this  acute 
stage  has  passed  the  organisms  disappear,  the  temperature 
falls,  the  severity  of  the  symptoms  abates,  and  there  is  an 
intermission,  during  which,  at  the  beginning  of  the  attack,  the 
patient  may  appear  in  good  health.  Although  the  blood  dur- 
ing an  intermission  may  appear  under  the  microscope  to  be 
ab.solutely  free  from  the  parasites,  its  inoculation  into  suscep- 
tible animals  will,  as  a  rule,  produce  the  di.sease.  The  blood 
of  surra  affected  horses  loses  its  power  of  transmitting  the  dis- 
ease by  inoculation  in  about  eighteen  hours  after  death. 


402  SURRA 

Under  the  microscope,  these  parasites  are  detected  in  a 
drop  of  blood  by  an  irregularly  intermittent  and  characteristic 
qnivering  of  some  of  the  red  blood  corpuscles,  which  become 
much  altered  in  form.  The  leucocytes  remain  unchanged  in 
appearance.  After  a  further  and  careful  examination  of  this 
slightly  quivering  blood  a  minute  thread-like  organism  with 
eel-like  movements  emerges  from  the  mass  of  corpuscles.  It 
may  be  seen  apparently  tugging  with  all  its  might  at  a  red 
corpuscle  endeavoring  to  detach  it  from  its  rouleau.  The 
question  of  the  manner  in  which  these  parasites  interfere  with 
the  health  of  the  affected  animal  has  not  yet  been  settled. 
When  they  are  outside  the  animal  body  and  in  a  dry  state, 
they  are  killed  or  rendered  inert  by  prolonged  atmospheric 
action. 

The  period  of  incubation  seems  to  be  liable  to  great  varia- 
tion. It  may  be  put  from  six  to  eight  days  after  inoculation 
or  ingestion  of  blood  taken  from  an  animal  suffering  from 
surra.  It  appears  from  Lingard's  investigation  that  the 
period  of  latency  may  be  prolonged  to  thirteen  days,  if  the 
blood  used  for  inoculation  has  been  taken  from  a  dead  animal. 
When  the  parasites  have  been  given  in  water,  by  the  mouth, 
symptoms  of  surra  may  not  appear  for  even  seventy-five  days. 
We  have  no  exact  data  for  determining  the  time  required  for 
the  disease  to  manifest  itself  under  natural  conditions  from 
drinking  surra  contaminated  water. 

i^  313.  Means  of  transmission.  The  contagium  of 
surra  is  fixed  and  can  be  conveyed  only  by  inoculation  or 
ingestion.  Stagnant  water  and  grass  growing  on  recently 
inundated  land  are  said  to  form  favorable  resting  places  for 
this  organism. 

Lingard  considers  the  ingestion  of  stagnant  water  and  of 
grass  from  land  subject  to  inundations  a  source  of  infection. 
Salmon  and  Stiles  do  not  think  this  method  of  infection  is 
sufficiently  proven  to  look  upon  it  seriously.  Liugard  stands 
almost  alone  in  the  belief  that  infection  can  take  place  through 
healthy  mucosae. 

The    most    coumion    demonstrated    natural    methods    of 


SYMPTOMS  403 

transferring  the  virus  from  infected  to  non-infected  animals  is 
by  means  of  insects,  especially  the  biting  fiies.  Of  the  flies, 
the  tsetse-fly  {G/ossina  mors/fa?is)  is  reported  to  be  the  most 
important.  Musgrave  and  Clegg  conclude  concerning  the  role 
played  by  flies  in  transmitting  this  disease  that  "  it  has  thus 
far  been  conclusively  shown  that  the  tsetse-fly  {G/ossma 
morsifa?is),  at  least  one  other  variety  of  (r/ossmi,  Stomoxys 
calcib'ans,  Miisca  brava  if),  Taon,  and  at  least  one  variety  of 
Tabani  transmit  the  virus.  All  other  biting  insects  have 
been  looked  upon  with  suspicion,  but  absolute  proof  of  trans- 
mission by  them  has  not  been  furnished."  The  theory  as  to 
the  method  of  transferring  the  parasite  is  that  it  is  purely 
mechanical,  although  some  have  thought  the  Trypanosoma 
passed  through  one  phase  of  its  life  cycle  in  the  fly. 

The  spread  of  the  disease  from  one  locality  to  another  is 
caused  by  the  introduction  of  animals  carr3'ing  the  parasite. 

^  314.  Symptoms.  The  symptoms  as  given  by  Lingard 
are  as  follows:  "The  chief  symptoms  are  the  occasional 
appearance  of  an  urticarial  eruption,  generalized  or  localized, 
closely  following  the  first  rise  of  temperature,  but  w-hich  may 
make  its  appearance  at  any  time  during  the  course  of  the 
disease  ;  then  the  presence  of  petechiae  on  the  mucous  mem- 
branes, chiefly  that  covering  the  membrana  nictitans,  lachry- 
mation  and  the  exudation  of  a  semi-gelatinous  material  into 
the  subcutaneous  and  other  connective  tissues.  There  is  rapid 
wasting  and  great  weakness,  although  in  the  majority  of  cases 
the  appetite  remains  good  throughout,  no  matter  how  high 
the  fever.  There  is  extreme  pallor  of  the  visible  mucous 
membranes,  and  this  is  followed  at  a  later  period  by  yellow- 
ness. From  first  to  la.st  there  is  progressive  anemia  ;  the 
blood  at  first  presents  a  normal  character,  but  after  a  varying 
period  of  time  it  undergoes  marked  changes.  The  white  cor- 
puscles are  increased  in  number  and  the  red  corpuscles  usually 
cease  to  form  normal  rouleaux,  lose  their  individuality  and  run 
together  forming  irregular  masses.  They  are  at  first  dark, 
but  gradually,  as  the  disease  advances,  almost  entirely  lose 
their  coloring  matter  and  become  pale." 


404  SURRA 

The  respective  duration  of  the  paroxysms  and  intermis- 
sions is  very  irregular.  Lingard  puts  it  down  as  from  one  to 
six  days.  He  states  that  in  a  few  experimental  horses  the 
paroxysms  lasted  from  eighteen  to  twenty-two  days. 

77/^  flf?^ra//^;z  of  the  disease  is,  according  to  Gunn,  about 
fifty-two  days.  In  the  Philippine  Islands  the  duration  in 
horses  is  from  fourteen  days  to  three  months.  The  prognosis 
is  always  unfavorable,  the  mortality  in  most  species  of  animals 
being  100  per  cent.      In  cattle  a   variable    percentage    recover. 

^  315.  Morbid  anatomy.  As  a  rule  there  is  great 
emaciation,  enlargement  of  the  liver  and  spleen,  petechiae  on 
various  internal  organs.  A  yellow  or  amber-colored  jelly-like 
exudation  occurs  in  the  connective  tissue  of  the  throat,  chest 
and  abdomen,  about  the  muscles  and  other  tissues,  and  espec- 
ially around  the  base  of  the  heart.  The  lungs  often  show 
signs  of  inflammation.  The  mucous  membranes  and  other 
tissues  are  frequently  tinged  yellow  by  the  coloring  matter  of 
the  bile. 

It  has  been  stated  that  the  hide  is  often  removed  with 
difficulty.  In  the  areas  corresponding  to  the  edema  dur- 
ing life  are  found  yellowish-tinged,  gelatinous  infiltrations. 
The  serous  membranes,  especially  the  peritoneum  and  pleura, 
often  show  flakes  of  plastic,  fibrous  material.  These  are  es- 
pecially numerous  over  the  liver.  All  of  the  organs  have  a 
dry,  pale  appearance.  There  are  numerous  sub-serous  hemor- 
rhages, particularly  on  the  right  side  of  the  heart  and  over  the 
lower  portion  of  the  lungs.  The  lymphatics  are  in  general 
somewhat  enlarged,  often  markedly  so.  The  heart  muscle 
shows  parenchymatous  changes,  in  degree  depending  some- 
what on  the  duration  of  the  disease. 

In  some  of  the  lower  animals  the  scrotum  and  even  the 
testicles  in  the  male  and  the  vulva  in  the  female  are  greatly 
swollen,  and  in  the  male  rabbit  the  tension  may  be  so  great  as 
to  rupture  the  scrotum.  Small  preputial  or  labial  ulcers  are 
not  uncommon. 

Steel  noticed  ulceration  of  the  stomach  in  about  two-thirds 


MORBID    ANATO-AIV  405 

of  his  cases  among  mules  in  Burma.  In  India  this  ulceration 
has  not  been  observed  among  horses  as  a  sequence  of  surra. 
In  the  Philippines  changes  in  the  intestine  due  to  anemia  with 
occasional  ulcers  are  reported. 

The  clinical  aspect  of  surra  is  esseutialh'  one  of  progres- 
sive anemia,  accompanied  b}-  parox3-sms  and  intermissions, 
during  both  of  which  there  is  a  natural  decrease  in  the  number 
of  the  red  blood  corpuscles  and  in  the  amount  of  hemoglobin 
in  the  blood,  with  consequent  anemia  of  the  visible  mucous 
membranes. 

The  importance  of  this  disease  renders  it  desirable  to 
reprint  "A  preliminary  note  on  a  parasitic  disease  of  horses," 
by  Capt.  Allen  M.  Smith  and  Dr.  J.  J.  Kinyoun,  from  the 
Army  Pathological  Laboratory,  Manila,  October  17,  1901,  as 
it  gives  a  good  idea  of  the  appearance  of  the  disease.  The 
accompanying  photograph  showing  trypanosoma  w'as  taken  by 
Smith  and  Kinyoun  at  that  time. 

"On  October  15,  1901,  information  was  given  by  J.  W.  Jobbing, 
Assistant  Bacteriologist  of  the  Board  of  Health  of  Manila,  that  an  epi- 
demic sickness  of  an  undetermined  nature  was  now^  prevailing  in  this 
city,  and  also  that  he  had  just  taken  a  specimen  of  blood  from  a  sick 
animal  which  on  examination  revealed  the  presence  of  a  parasite, 
whether  this  was  accidental  or  was  the  causative  agent  of  the  disease  in 
question,  he  was  unable  to  sa^-.  On  investigation  and  inquiry  it  was 
learned  from  the  Veterinarian  in  charge  of  the  corral  of  the  Quarter- 
master's Department,  and  from  the  City  Veterinarian,  that  there  was 
now.  and  had  been,  a  fatal  epidemic  among  the  horses  in  Manila,  the 
Quarter-master's  Department  having  lost  over  200  within  the  i)ast  four 
months. 

"  One  of  the  corrals  was  visited  by  us  on  the  15th  inst. ,  where  we 
were  shown,  by  the  \'eterinarians  in  charge,  20  horses  and  mules,  ill 
with  an  undetermined  disease.  These  animals  presented  the  several 
stages  of  the  malady,  some  were  quite  recently  attacked,  while  others 
had  been  ill  for  over  tw'o  months. 

"The  symptoms  first  noticed  are  :  impairment  of  appetite,  constipa- 
tion, fever  and  thirst.  These  are  followed  within  a  few  days  by  a  rapid 
and  progressive  emaciation. 

"  The  temperature  for  the  first  few  days  ranges  from  104"^  to  107^  F., 
the  pulse  is  full  and  strong.  This  may  be  termed  the  acute  stage.  Then 
begins  an  asthenic  state,  which  may  terminate  fatally  within  a  variable 


406  SURRA 

period,  or  by  a  slow  convalescence.  During  this  stage  usually  within 
lo  days  after  the  onset,  there  appears  a  commencing  oedema  above  the 
belly,  involving  the  soft  parts,  coincident  with  this,  or  soon  after,  the 
cedema  extends  to  the  feet  and   legs.       The   pulse  becomes  rapid,  weak 


-0^  ^Ifc^^^. 


• 


#- 


Fig.   107.      Photograph    of  blood  of  horse  coiilaining    Tiypanosoma. 
Taken  by  Smith  and  k'iiiyoiiii. 

and  dichrotic,  the  respiration  increased,  shallow  and  jerky,  the  gait 
staggering.     Emaciation  is  rapid  and  extreme. 

"  The  disease  has  a  tendency  to  relapse,  this  may  occur  at  any  time, 
even  after  convalescence  appears  to  have  been  fully  established.  The 
relapses  are  invariabh-  fatal. 

"The  mortality  in  this  epidemic  has  been  about  75  per  cent  for 
American  horses  and  mules,  and  100  per  cent  for  native  ponies. 

"  The  gross  pathology  shows  serous  effusions  into  the  pleurte,  peri- 
cardium, and  sometimes  the  peritoneum.  There  is  also  a  serous  exudate 
into  the  cellular  tissue  of  the  legs  and  abdomen.  The  organs  are  pale, 
but  otherwise  normal  in  appearance. 

"  At  the  time  of  our  inspection,  five  acute  cases  were  examined,  the 
duration  of  the  attack  being  from  six  days  to  two  weeks.  All  these 
animals  presented  the  several  clinical  appearances  as  above  described. 

"Blood  specimens  were  taken  from  the  jugular  vein  of  each  and 
examined  microscopicall)-,  shortly  afterwards.       In  4  of  these  a  parasite 


M  OK  HID    ANATOKV  407 

was  demonstrable.  The  other  was  negative,  but  a  specimen  taken  the 
followiug  day  showed  the  presence  of  this  same  parasite. 

"  On  the  day  following,  specimens  were  obtained  from  12  others,  all 
chronic  cases,  with  the  result  of  finding  this  same  parasite  in  the  blood 
of  four.  In  three  there  were  very  few,  whilst  in  the  fourth  they  were 
present  in  great  numbers,  as  many  as  20  could  be  seen  in  one  microscope 
field.  The  animal  from  which  the  specimen  was  taken  had  suffered  a 
relapse 

"  It  would  appear  that  the  parasite  may  disappear  from  the  peri- 
pheral circulation,  or  exists  there  in  such  few  numbers  that  it  is  not 
easilj'  demonstrable,  after  the  acute  stage  has  passed.  It  would  re(|uire 
repeated  blood  examination  to  decide  this  point. 

"  Description  of  the  parasite.  The  parasite  resembles  a  whiplike 
worm,  having  much  the  appearance  of  the  Trichocephalus  Dispar,  its 
length  is  from  10  to  14  mikrons,  and  is  from  i  to  1.2  mikrons  in  diameter 
through  its  body,  the  neck  is  nearly  ',  its  length,  tapering  gradually  to 
a  point  representing  the  mouth  (?).  It  has  a  limiting  membrane,  which 
is  well  defined,  the  contour  is  in  most  cases  symmetrical  but  in  some 
the  body  line  is  (juite  irregular.  The  larger  part  of  the  parasite  (body) 
contains  granular  material  and  clear  spaces,  which  latter  vary  in  size 
and  number;  they  are  ijregularly  distributed,  and  may  encroach  on  the 
wall  so  as  to  cause  irregular  outline.  The  granular  material  does  not 
extend  to  the  neck. 

"  The  parasite  is  activel}-  motile,  having  both  a  vermicular  (con- 
tractile)  and  spiral  movement.  It  moves  forward  in  a  very  peculiar 
manner,  the  long  whiplike  process  is  thrust  forward  by  a  spirillar 
motion,  followed  by  a  contraction  of  the  body. 

"  We  have  not  so  far  been  able  to  determine  its  intimate  structure, 
further  than  the  limiting  membrane,  and  the  protoplasmic  substance  of 
the  body. 

"  Two  sizes  of  the  parasite  have  been  seen  in  all  the  specimens  ex- 
amined, the  larger  appears  to  be  more  numerous,  and  contains  consider- 
ably more  granular  material  than  the  smaller,  and  usually  two  or  more 
vacuoles.  Whether  these  two  sizes  represent  male  and  female,  has  not 
been  determined.  We  are  inclined  to  believe  from  our  observations, 
that  they  do  not  represent  the  male  and  female,  because  we  have  ob- 
served in  more  than  half  the  fresh  specimens,  the  joining  of  a  large  and 
small  parasite  in  such  a  way  as  to  appear  to  be  something  more  than 
accidental. 

"The  pathological  changes  caused  by  this  parasite  is  a  rapid  de- 
struction of  the  red  blood  cells,  causing  an  acute  anamia.  The  changes 
occur  in  the  blood  coincident  to  the  invasion  of  the  parasite.  In  one 
horse    which    had   been  ill  seven    davs,  the  red   blood  cells    numbered 


408  SURRA 

3,500,900,  the  white  14,500.  In  another,  ill  six  weeks,  the  red  blood 
cells  were  3,200,000,  and  the  white  were  13,900.  The  blood  of  a  healthy 
horse,  taken  as  a  comparison,  gave  red  blood  cells  6,900,000,  white 
9,Soo.  There  is  also  a  slight  diminution  in  the  amount  of  httmoglobin, 
about  85  per  cent. 

"  After  convalescence  has  been  fully  established,  no  parasite  can  be 
found,  the  blood  gradually  assumes  its  normal  constitution. 

"The  parasite  is  not  confined  to  the  blood,  as  it  can  be  demonstrated 
in  the  serous  effusions. 

"  It  is  quite  easy  to  detect,  all  that  is  necessary  is  to  make  a  micro- 
scopical examination  of  fresh  bJood  films,  a  },  in.  objective  will  suffice. 
Dried  films,  fixed  and  stained  with  any  of  the  nuclear  dyes. 

"  The  organism  appears  to  be  a  strict  parasite.  It  lives  but  a  short 
time  after  removal  from  the  body,  the  longest  time  which  it  has  been 
kept  alive  in  blood  serum  was  not  more  than  ten  hours. 

"The  parasite  has  many  of  the  properities  in  common  with  the 
filaria,  and  resembles  more  nearly  that  of  filaria  perstans.  only  it  is 
smaller,  and  its  movements  dissimilar.  Yet  on  the  other  hand,  the 
clinical  history  of  animals  infested  by  it,  the  changes  occurring  in  the 
blood,  the  lesions  observed  in  post-mortem,  point  very  strongly  towards 
its  classification  with  the  spirochx-te. 

"  The  mode  of  transmission  has  not  yet  been  studied.  It  does  not 
appear  to  be  highly  contagious,  as  it  does  not  appear  to  spread  from  one 
to  another,  even  under  the  most  favorable  circumstances. 

"  It  more  nearly  resembles  malaria  in  this  respect.  It  is  more  than 
probable  that  its  extra  corporeal  state  is  different,  or  another  supposition 
equally  tenable,  is  that  its  intermediate  host  is  some  insect,  such  as  the 
fly  or  mcsquilo." 

§  316.  Differential  diagnosis.  Surra  is  to  be  differen- 
tiated from  anthrax  and  the  other  trypanosoma  diseases.  A 
history  of  the  case  or  outbreak  together  with  the  chronic 
course  and  intermittent  temperature  in  surra  will  usually 
suffice  to  determine  the  nature  of  the  disease.  A  positive 
diagnosis  can  easily  be  made  in  the  horse,  in  a  majority  of 
cases,  by  a  microscopic  examination  of  the  blood.  The  try- 
panosoma are  readily  observed,  and  usually  they  are  in  suffi- 
cient numbers  to  be  quickly  seen.  In  a  suspicious  case,  where 
the  organisms  are  not  found,  the  examination  should  be 
repeated  daily  or  small  animals  inoculated  with  the  blood.  For 
this  inject  about  i  c.c.  of  the  blood  into  the  abdominal  cavitv 


PRKVKNTION 


409 


of  a  dog.  In  a  few  days  the  trypanosoma  will  be  found  in 
the  usual  way  if  the  disease  is  surra.  Although  this  requires 
some  time  the  importance  of  a  positive  diagnosis  demands  that 
it  should  be  done. 

Surra  may  be  complicated  with  broncho-pneumonia,  Rin- 
derpest and  tuberculosis  (especially  in  cattle),  foot  and 
mouth  disease,  pseudo-actinomycosis,  neoplasms  and  septi- 
cemias as  yet  little  understood. 

If  no  history  or  symptoms  are  known,  the  diagnosis  can 
be  made  post-mortem  from  the  bacteriological  examination  of 
the  tissues  or  blood,  as  Bacf.  aiifhracisxi^  readily  found  in  cases 
of  anthrax. 

^  317.  Prevention.  The  importation  of  animals  from 
infected  countries  should  be  prohibited.  If  the  disease  gains 
entrance,  the  infected  animals  should  be  destroyed.  In  fram- 
ing regulations  for  quarantine  particular  attention  should  be 
paid  to  the   wild  animals  and  to  circus  animals. 

lyingard  found  that  arsenic  has  a  decided  effect  in  dimin- 
ishing the  number  of  surra  organisms  in  the  blood  of  affected 
animals.      Thus  far  serum  therapy  is  not  successful. 

From  the  latest  results,  it  is  very  clear  that  infected 
animals  must  be  destroyed  and  the  healthy  ones  protected 
from  the  bites  of  insects. 

REFERENCES. 

1.  BtTKKE.  vSurra  or  progressive  pernicious  ana-mia.  /W.  Jour. 
London.  Vol.   XXV,  1887. 

2.  Durham.      Tsetse  disease.        Veterinarian.  \o\.    LXXMiSgS). 

3.  Dl'RRANT.  a  trypanosoma  fonnd  in  blood  of  cattle  in  India. 
Jour.  Comp.  Path,  and  'I'heia.     \'o\.  X\'II  {1904),  p.  209. 

4.  EvAXS.  Report  on  surra  disease  in  the  Dera  Ismail  Khan  Dis- 
trict.     18S0.     Military  Department. 

5.  Evans.  On  a  horse  disease  in  India  known  as  "  surra,"  proba- 
bly due  to  a  Hiumatozoon.  I'et.  Jour.  Loiidoii.  \"ol.  XIII  (1881), 
July,  Aug.,  Sept.,  Nov. 

6.  H.ASSAi.i..     Bibliography     of   surra    and    allied    trypanosomatic 


41°  DOURINE 

diseases.     Bulletin  No.  42,  U.  S.    Bureau    of  Animal   Industry.   1892, 
p.  132. 

7.  Kanthack,  Durham  and  Blandford.  On  nagana  or  tsetse 
fly  disease.  Report  made  to  the  tsetse  fly  committee  of  the  Royal  so- 
city,  etc.     Proc.   Royal  Soc.  London,  \'ol.  LXIV,  p.  100. 

8.  LixOtARD.     Report  on  horse  surra.     1893.     (Bombay.) 

9.  LiNGARD.  Report  on  "surra"  in  equines,  bovines,  buffaloes 
and  canines,  etc.     Rec.  de  rued.  vet.  Par.  S.     Vol.  X'lII,  p.  377. 

10.  MuSGRAVE  AND  Ci,KGG.  Trypanosoma  and  Trypanosomiasis, 
with  special  reference  to  surra  in  the  Philippine  Islands.  No.  5.  I!u- 
reau  0/ Government  Laboratories,  Manila,  1903. 

11.  Ml'SGRAve  AND  Clfgg.  Report  of  the  Superintendent  of  Goi- 
ernment  Laboratories  in  the  Philippine  Islands,  1903. 

12.  NocARD.  Sur  les  rapports  qui  existent  entre  la  dourine  et  le 
surra  ou  le  nagana.     Camp.  rend.  Soc.  de  Biol.     Vol.  LIII  (1901). 

13.  Ranking.  A  preliminary  note  on  the  nature  and  pathology  of 
the  disease  known  as  "  .surra  ''  affecting  horses  and  mules  in  India.  Vet. 
Jour.  London,  Vol.  XXXII  (1891  ). 

14-  Salmon  and  vStiles.  Emergency  report  on  surra.  Bulletin 
No.  42,  L'.  S.  Bureau  0/  Animal  Industry,  1892. 

15.  Schilling.  Bericht  iiber  die  Surra-Krankheit  der  Pfenle, 
Centralblattf.  Bakteriologie  u.  Parasit.     Bd.  XXX  \\^2),  p.  545, 

16.  Smith  and  Kinvoun.  A  pliminary  note  on  a  parasitic  disease 
of  horses.     Army  Pathological  Laboratory,  Manila,  Oct.  17,  1901. 

17.  Steel.  On  relapsing  fever  of  equines.  Vet.  Jour.  London. 
Vol.  XXII  (  18S6). 

18.  Steel.  Report  upon  an  obscure  and  fatal  disease  among 
transport  mules  in  British  Burma.      1885. 

19.  Stiles.  Trypanosoma  in  a  new  role.  Am.  Med.  Vol.  Ill 
(1902). 


DOURINE 


Sy?ionyiiis.  \'enereal  disease  of  solipeds;  equine  syphilLs; 
chancerou.s  epizootic;  breeding  paralysi.s;  epizootic  paraplegia: 
maladie  du  coit. 

§  318.  Characterization.  A  contagious  affection  of 
solipeds,  transmitted  by   copulation    and   attended    by  specific 


HISTORY  411 

lesions  of  the  generative  organs  and  nervous  system,  such  as 
local  venereal  swellings,  chancerous  ulcers  and  cicatrices,  de- 
mentia and  paralysis. 

The  disease  is  essentially  an  equine  one,  although  the  fol- 
lowing species  are  susceptible  to  experimental  inoculation, 
namely:  dogs,  rabbits,  rats,  mice  and  asses.  While  the  horse 
shows  the  greatest  susceptibility,  the  ass  is  comparatively 
resistant  to  the  infection. 

>:^  319.  History.  Dourine  seems  to  have  first  been 
recognized  in  Algeria.  It  was  first  clearly  described  in  1796 
by  Amnion  who  found  it  in  the  royal  stud  at  Trakchnen  in 
Northern  Prussia.  We  have  later,  1801  and  1807,  descrip- 
tions of  the  disease  in  the  same  locality.  It  was  found  in 
Bomberg  in  1817  to  1820,  in  Austria  and  Bohemia  in  1821-8, 
in  Syria  in  182 1,  in  Switzerland  in  1830,  in  France  in  1830-32, 
in  Siberia  in  1833-40,  in  Italy  in  1836,  in  Russia  in  1843,  in 
Poland  in  1830-40,  in  Algiers  in  1847-55.  In  Syria  and  Asia 
generally  it  is  reported  to  appear  perennially. 

It  is  not  known  to  have  invaded  Belgium,  Scandinavia, 
England,  South  America  or  Australia.  All  indications  point 
to  Asia  and  Northern  Africa  as  the  home  of  the  disease  where 
it  still  appears  perennially. 

It  was  found  in  De  Witt  County,  111.,  in  1882.  The  first 
animal  showing  the  disease  was  a  brown  stallion  that  had  been 
imported  from  France.  In  this  locality  it  spread  to  a  consid- 
earble  number  of  breeding  mares  and  stallions.  The  di.sease 
was  very  largely  stamped  out  of  that  region  by  a  rigid  quar- 
antine of  diseased  and  exposed  animals.  Some  exposed  ani- 
mals had.  however,  left  the  district,  and  it  is  not  surprising 
that  isolated  centers  of  infection  are  occasionally  found. 

i^  320.  Etiology.  ThanhofTer  found  in  the  blood,  vagi- 
nal mucus,  testicle,  semen,  spinal  fluid  and  roots  of  the  dorsal 
and  lumbar  nerves,  bacteria,  especially  streptococci  and  less 
constantly  bacilli,  to  which  he  attributed  the  cause.  More 
recently  Schneider  and  Buffard  have  apparently  demonstrated 
that  one  of  the  Trypanosoma  is  the  specific  pathogenic  agent. 


412 


Rouget  in  1896,  described  a  trypanosoma  found  in  the 
blood  of  a  horse  suffering  from  dourine,  and  for  over  two  years 
continued  the  study  of  this  organism  in  susceptible  animals. 
Wasilewsky  and  Senn  confirmed  Rouget 's  work,  and  deter- 
mined the  pathogenic  action  of  this  trypajiosoma  for  the  horse, 
passing  it  through  other  animals  and  back  to  the  horse,  repro- 
ducing the  disease.      Laveran  and  Mesnil  (igoi)  proposed  the 


Fig.   108.      Tr.  eqiiiperdmii.     1 ,  i/i  the  blood  0/ a  mouse  four  days  after 
inoculation,  _->,  same  blood  eight  days  after  inoculation  {after  Rouget). 


name  Tr.  roitgetii  for  the  parasite  of  dourine.  Doflein  named 
it  Tr.  equiperdiim ,  which  is  the  name  used  by  Salmon  and 
Stiles. 

In  its  morphology  and  evolutionary  forms,  the  trypano- 
soma of  dourine  has  not  been  shown  to  differ  from  that  of 
surra.  The  granule  form,  the  spherical,  the  club  shaped  or 
pyriform  bodies,  the  fusiform  with  more  or  less  stellate  group- 
ings seem  to  be  generic  characteristics.  Baldrey  states  that  it 
is  smaller  than  the  Trypanosoma  of  Surra.  The  specific  dis- 
tinction is  found  in  the  pathogenesis  as  shown  by  the  two 
diseases  (surra  and  dourine). 

In  the  active  stages,  the  parasite  is  usually  found  abund- 
antly in  edematous  fluid,  the  blood,  semen,  milk,  vaginal 
secretions  and  the  erosions  of  the  vaginal  mucosa  and  penis. 
During  intermissions,  however,  and  in  the  absence  of  local 
lesions,  the  parasites  are  not  found  in  the  blood  on  micro- 
scopic   examination,   yet    the    inoculation    of  the    blood  into 


KTIOLOCiY  4  '  3 

a  dog  will  usually  produce  the  disease.  The  parasite  disap- 
pears from  the  blood  and  tissues  very  rapidly  after  death, 
so  that,  to  prove  successful,  inoculations  should  be  made 
from  an  infected  individual  before  or  immediately  after  death. 
Thev  are  not  affected  after  forty-eight  hours. 

Schneider  and  Buffard,  Nocard  and  others  found  the  try- 
panosoma  in  the  blood  and  exudates  of  horses,  asses  and  dogs 
Lffering  from  dourine.     They    failed  to  find  it  in  the  same 
localities  in  animals  of  the  same 
species    which     were    free    from 
dourine.        The    infected    blood 
preserved  for  24  hours  in  sealed 
glass  tubes,  and  then  inoculated 
into    dogs    produced    character- 
istic symptoms  and  lesions  with 
many  trypanosoma  in  the  blood. 
Inoculation  into  two  other  dogs, 
with  the  same  material,    but  at 

the  end  of  48  hours,  produced  a  ^^^^  ^^^  jy^osoma  o/dou- 
slight  transient  hyperemia  only,  ^,.^^^,  -^^  ^j^^,  process  of  division 
without  local  lesions  or  propaga-  Rafter  Ugnicres). 

tion  of  the  parasite  in  the  blood.  • 

The  blood  from  the  same  animal  inoculated  after  filteen  da^s 
eave  negative  results. 

Baldrey  found  Romanowsky's  and  Wright's  modifications 
of  Leishman-s  method  the  best  methods  for  staining    the    try- 
panosoma ;  the  latter  is  very  useful  and  handy,  as  no   mixing 
of  solutions  is  necessary  and  no  fixing  required. 
The  following  is  Romanowskf  s  Stain  : 

STOCK   SOLUTION    NO.    I. 

„,                                                     _         I   part 
Hochsfs  Medicinal  Methylene  Blue 0.5  parts 

Sodium  Carbonate  pure ' ^^^  p^^^^ 

Distilled   water 

Place  this  solution  in  an  incubator  at  37°  C.  for  two   or   three   da, 
when  a  purple   color  will  be  noticed  at   the   edges  of   the    ^^^ 
depends  m>on  the  formation  of  a  new  red  color-methylene  red-vUnch 
crbinedUheosin  forms  the  active  principle  of  the   stain   and    has   a 


414  DOUR INK 

particular     affinity    for   chromatin.       Unless   this    polychroniatophylic 
change  takes  place  the  solution  is  useless. 

STOCK    SOLfTION    NO.    2. 

Eosin I  part 

Water 1000  parts 

For  staining,  the  stock  solutions  are  separately  diluted  with  water, 
5  parts  of  stock  solution  to  100  parts  of  water. 

In  order  to  obtain  a  smear,  prick  the  center  of  the  plaque  and  take 
a  drop  of  blood  on  a  slide,  which  should  be  chemically  clean,  having 
been  taken  from  an  alcohol  bottle  and  dried  with  a  clean  piece  of  art 
muslin.  Then,  either  in  the  ordinary  way  with  a  piece  of  cigarette 
paper,  make  a  thin  even  smear  over  the  slide,  or,  as  an  easier  and 
equally  efficient  method,  take  a  perfectly  clean  flat  large-sized  needle 
and  place  it  edgeways  on  the  drop,  when  the  capillary  attraction  of  the 
needle  will  cause  the  blood  to  stream  right  across  the  slide  ;  then 
evenly  and  gently  draw  the  needle  down  the  length  of  the  slide,  and  a 
very  even  smear  may  be  obtained.  (Juickly  dry  the  smear  in  the  air  by 
waving  rapidly  about,  which  prevents  the  red  corpuscles  from  crenat- 
ing ;  the  slide  can  then  be  kept  indefiniteh'  or  used  at  once.  The 
advantages  of  using  a  slide  instead  of  a  cover-glass  are  that  3-ou  get  a 
much  larger  field  on  which  to  work,  it  is  much  more  easily  manipulated 
and  it  can  be  kept  without  any  mounting.  Place  the  film  in  absolute 
alcohol  or  alcohol  and  ether,  for  fifteen  minutes  to  half  an  hour,  to 
fix.  This  coagulates  the  albumen  and  makes  a  permanent  film  in  which 
the  corpuscles  and  organisms  are  retained  Remove  from  the  alcohol, 
wash  in  water,  and  then  apply  the  stain.  This  is  made  by  mixing  equal 
parts  of  the  above  two  solutions,  freshly  prepared,  in  a  small  glass 
measure  or  porcelain  dish.  It  is  important  that  the  admixture  should 
be  as  fresh  as  possible.  Apply  the  stain  to  the  whole  of  the  film  and  let 
it  remain  for  seven  to  ten  minntes  ;  wash  in  water  and  dry  in  the  air, 
no  heat  being  applied.  The  red  corpuscles  may  have  a  bluish  tinge, 
which  may  be  removed  by  further  washing.  If  the  blood  platelets 
appear  bluish  the  film  requires  further  staining  ;  they  shoiild  appear  as 
ruby-red  granular  bodies.  By  continuous  application  of  water  the  stain 
may  be  washed  out,  but  the  film  maj-  always  be  stained  over  again. 

By  this  stain  the  protoplasm  of  the  trypauosome  is  stained  blue,  the 
nuclear  chromatin  a  carmine  violet,  and  the  flagellum  and  centrosome  a 
brilliant  red.  The  red  corpuscles  will  be  a  pinkish  colour,  and  the  vari- 
ous forms  of  leucocytes  will  be  well  differentiated.  In  examining  the 
smear,  time  may  be  saved  by  looking  along  the  edge  of  the  film,  as  it  is 
here  that  the  parasites  will  be  most  numerous  if  they  are  present,  as 
they,  being  like  the  leucocytes  of  less  density  than  the  rest  of  the  blood, 
tend  to  run  to  the  periphery  when  the  smear  is  made. 

A  film  made  in  this  way  requires  no  cover- glass,  but  if  the  cedar  oil 


SYISIPTOMS 


415 


is  left  on  it  tends  to  withdraw  the  color  ;  lio\\ever,  if  it  be  carefully 
blotted  and  wiped  off  with  a  soft  ra.y  after  use  the  film  may  be  kept 
indefinitely. 

§  321.  Symptoms.  The  first  local  changes  in  the  geni- 
tal organs  begin  after  a  period  of  incubation,  according  to 
Maresch,  of  from  eight  days  to  two  months.  The  first  symp- 
tom in  the  stalHon  consists  in  the  swelling  of  the  glans  penis. 
Reddish  spots,  vesicles  and  ulcers  may  occur  on  the  outer  sur- 
face of  the  organ.  The  meatus  urinarius  is  reddened  and 
swollen  and  exhibits  a  raucous  discharge.  The  animal  has  a 
continuous  desire  to  micturate  and  frequently  manifests  sexual 
excitement.  The  swelling  also  spreads  from  the  penis  to  the 
sheath  and  scrotum  in  which  case  the  testicles  become  in- 
flamed. Finally,  the  inguinal  glands  and  lymph  vessels 
become  involved.  These  local  affections  may,  as  the  disease 
advances,  almost  entirely  disappear.  In  some  cases  the  ex- 
ternal changes  are  absent,  as  the  mucous  membrane  of  the 
urethra  is  first  affected,  the  only  visible  sj'mptoms  being 
strangury  and  a  mucous  discharge  from  the  urethra. 

In  mares,  the  disease  begins  with  a  dough}' or  tense  swell- 
ing of  the  pudenda,  which  frequently  spreads  to  the  udder  and 
inner  surface  of  the  thighs.  The  mucous  membrane  of  the 
vagina  is  red  in  spots  and  swollen,  sometimes  thickened  by 
gelatinous  elevations  and  covered  with  a  turbid  and  orange 
colored  secretion.  Sometimes  nodules,  vesicles  and  ulcers  are 
observed  on  the  mucous  membrane.  They  are,  however,  fre- 
quently absent.  In  mares,  the  local  manifestations  are  often 
insignificant.  The  mucous  membrane  in  the  neighborhood  of 
the  clitoris  is  more  congested  than  at  other  points  and  the  cli- 
toris itself  is  swollen  and  erect.  It  is  devoid  of  pigment  and 
unnaturally  dry.  Williams  states  that  this  depigmentation  is 
"  peculiar  and  characteristic."  The  spots  of  discoloration  are 
not  caused  by  previous  ulcers.  At  the  same  time  affected 
mares  show  excessive  sexual  excitement.  They  frequently 
suffer  from  strangur}-  and  after  considerable  straining  urine  is 
discharged  in  small  jets.  In  his  report  on  the  Illinois  out- 
break, Williams  states  that  in    mares,    "  The  open  vulva  and 


41 6  DOURIXE 

enlarged,  protruding,  unnaturally  dry  clitoris,  especially  in 
young  and  otherwise  healthy  mares  is  quite  pathognomonic." 

Instead  of  urine  small  quantities  of  sticky,  discolored 
mucus  are  discharged.  The  animals  incessantly  shake  their 
tails  and  open  and  close  the  vagina  in  rapid  succession,  show- 
ing the  clitoris  as  mares  do  in  season.  The  discharge  often 
exerts  a  corrosive  action  on  the  tail  and  legs.  In  severe  cases 
the  neighboring  lymph  glands  become  inflamed  and  swollen  as 
well  as  the  udder,  on  which  abscesses  may  appear.  The 
swelling  may  even  extend  to  the  hypogastrium. 

The  general  symptoms  develop  only  after  weeks  or  even 
months;  their  appearance  is  often  delayed  until  the  local 
symptoms  have  disappeared.  At  first  the  animals  are  de- 
pressed and  weak,  they  frequently  continue  to  lift  up  their 
hind  feet,  alternately,  so  as  to  try  to  avoid  putting  weight 
upon  them,  knuckle  on  their  fetlock  joints  and  lose  control 
over  the  movements  of  their  hind  legs  while  walking.  The 
temperature  is  not  so  high  as  in  other  forms  of  Trypanosma 
infection. 

It  is  reported  that  stallions  especially  suffer  from  an 
urticaria  in  the  form  of  sharply  defined,  round,  flat  eminences 
which  may  be  raised  the  breadth  of  a  finger  above  the  surface 
and  which  may  vary  in  size  from  two  to  four  centimeters  or 
more  in  diameter.  These  eminences  are  caused  by  a  serous 
infiltration  of  the  papillary  layer  of  the  skin  in  the  neighbor- 
hood of  a  small  artery  and  are  evidently  of  a  vaso-neurotic 
character.  They  often  appear  and  disappear  very  rapidly  and 
may  shift  their  position.  Usually  they  persist  for  several 
weeks  during  which  time  they  become  moderately  hard  and 
then  slowly  disappear.  Their  favorite  sites  are  the  croup, 
neck,  shoulders,  chest  and  abdomen. 

I,ater  in  the  course  of  the  disease,  a  progressive  paralysis 
of  the  hind  quarters  combines  with  excessive  emaciation.  The 
animal  has  a  staggering  gait  and  often  gives  way  on  the  pas- 
terns and  at  the  knees,  can  raise  itself  from  the  ground  only 
with  difficulty,  and  sometimes  falls  down  unexpectedly.  The 
affected  stallion  is  unable  to  cover,  as  he  can  neither  mount  a 


SYMPTOMS  417 

mare  nor  get  an  erection.  Some  patients  exhibit  permanent 
treml)lings  over  the  whole  body  or  local  paralysis  as  for  in- 
stance, that  of  the  lips,  ears  and  eyelids.  Hyperesthesia  of  the 
skin  is  observed  particularly  in  stallions  and  with  it  is  exten- 
sive pruritis,  so  that  the  animal  continually  rubs  itself,  bites 
the  affected  parts  and  thus  produces  extensive  sores  on  the 
skin.  The  patient  becomes  extremely  emaciated  especially  in 
the  hind  quarters  so  that  the  outlines  of  the  pelvic  bones  and 
ribs  become  very  prominent.  The  skin  becomes  dry,  the  hair 
is  ruffled  and  loses  its  gloss.  Some  animals  manifest  pain  when 
the  lumbar  region  is  pressed.  The  senses  become  more  and 
more  blunted  and  the  eyes  a.ssume  a  staring  and  expressionless 
appearance.  As  the  end  approaches  the  patient  persistently 
maintains  a  recumbent  po.sition  and  finally  dies  from  the  effect 
of  secondary  lesions  such  as  hypostatic  inflammation  of  the 
lungs,  septicemia  or  perhaps  general  cachexia.  Sometimes  in 
the  final  stage  the  patient  suffers  from  nasal  catarrh  with 
swelling  of  the  submaxillary  glands  and  conjunctivitis.  Severe 
internal  inflammation  of  the  eyes  has  been  observed.  The 
appetite  continues  longer  than  any  of  the  other  normal 
functions. 

Baldrey  has  divided  the  symptoms  into  three  different 
stages,  as  suggested  by  Nocard.  These  stages  are  distinct, 
and  may,  if  the  case  is  carefully  watched,  be  recognized  com- 
paratively easily.     They  are  : — 

Primary.  In  which  occur  the  local  manifestations  of  dis- 
charge and  urethral  irritation,  and  ulceration  of  the  penis  and 

sheath. 

Secoyidary.     In  which  the  exanthematous  eruptions  appear 

in  the  skin — the  .so-called  ' '  plaques  ' ' . 

Tertiary.     Characterized   by   the   formation   of  lesions  in 

the  central  nervous  .sy.stem,  and  by  nervous  di.sturbance  with 

ultimate  paraplegia. 

It  was  probably  on  account  of  these  three  periods  that  the 

older  writers  confounded   the  di.sease  with   syphilis,  and  it  is 

also  possible  that  the  ulcerations  and  chronic  enlargements  of 


4l8  DOURINE 

the  sheath  and  penis  gave  rise  to  the  idea  that  it    was   a    form 
of  localized  glanders. 

The  duration  of  the  disease  is  stated  b}-  Williams  to  extend 
from  three  months  to  as  many  years.  The  prognosis  is 
unfavorable. 

§  322.  Morbid  anatomy.  In  the  early  stages. there  are 
phlegmonous  or  edematous  swellings  of  the  sheath,  scrotum, 
penis  and  inguinal  glands  and  a  yellowish  liquid  effusion  into 
the  scrotal  cavity.  The  skin  covering  the  parts  may  show  a 
papular  or  vesicular  eruption  or  if  this  has  passed  a  mottling 
with  white  spots  shows  where  these  lesions  have  been.  Later, 
the  inguinal  glands  shrink  and  become  firm,  owing  to  the 
development  of  fibroid  tissue.  The  testicles,  which  are  either 
swollen  or  shrunken,  contain  foci  of  suppuration  or  caseation. 
The  connective  tissue  of  the  epididymis  and  the  cord  is  the  seat 
of  a  gelatinous  exudate.  The  walls  of  the  scrotum  may  be 
greatly  thickened  and  be  the  seat  of  abscesses  or  of  caseous 
degenerations.  In  advanced  cases  the  testicles  are  usually 
abnormally  small,  even  if  the  scrotal  mass  is  enormously  dis- 
tended. The  sheath  and  penis  may  be  the  seat  of  more  or  less 
numerous  ulcers  and  swellings.  Contraction  and  contortions 
of  the  penis  are  not  uncommon.  It  may,  how^ever,  retain  its 
normal  dimensions.  The  walls  of  the  lymphatics  in  the 
inguinal  region  may  be  the  seat  of  hyperplasia  ;  the  thickening 
causes  them  to  stand  out  like  cords  as  in  glanders.  In  the 
advanced  stages  the  muscles,  especially  those  of  the  hind 
limbs,  become  pale  and  atrophied.  The  nerve  centers  under- 
go profound  changes  which  have  been  studied  by  Thanhoffer. 
The  pia  mater  in  the  affected  part  ot  the  spinal  cord  is  the 
seat  of  active  congestion  and  thickening.  The  central  canal 
of  the  cord  is  dilated  more  at  one  point  than  another,  contains 
more  than  the  normal  amount  of  liquid  and  the  neuroglia 
around  it  is  thickened  and  fibrous.  The  substances  of  the 
cord,  both  white  and  gray,  show  congestion,  blood  staining, 
and  points  of  softening  and  of  hyperplasia  of  the  neuroglia. 
The  nerve  cells  are  modified  in  various  ways,  some  being 
granular,  some  discolored  by  fine  granular  pigment,  some  hav- 


MORHID    ANATOMY  4I9 

ing  enlarged  and  multiple  nuclei  and  some  show  vacuoles. 
The  nerve  filaments  often  show  a  granular  degeneration 
extending  from  the  nerve  cell  to  the  axis  cylinder.  The  latter 
is  liable  to  be  varicosed  or  enormously  enlarged.  In  the 
affected  portion  of  the  cord,  leucocytes  are  numerous  and  there 
is  often  hyperplasia.  The  neuroglia  tends  to  increase,  and 
apart  from  the  foci  of  softening  tends  to  give  a  special  firmness 
to  the  substance.  The  subarachnoid  and  subdural  fluid  is 
increased  and  there,  may  be  at  the  roots  of  the  spinal  nerves, 
especially  in  the  dorsal  and  lumbar  regions,  a  gelatinoid  exu- 
date investing  the  nerve,  distending  the  connective  tissue 
beneath  the  neurilemma  and  even  occupying  the  interval 
between  the  nerve  filaments.  Sometimes  large  corpuscular 
bodies  are  found  between  the  nerve  fibers. 

Weber  and  Nocard  state  that  sections  show  cachexia  and 
hemorrhagic  softening  of  the  spinal  marrow.  The  parasites 
found  in  these  areas  and  in  the  serous  effusions  resemble  those 
of  surra  and  nagana. 

The  cerebral  meninges  are  congested  and  opaque.  Foci 
of  softening  are  by  no  means  uncommon  and  the  cerebral 
ventricles  contain  an  abnormal  quantity  of  fluid. 

The  bony  tissue  generall}^  has  lost  its  consistency  and  the 
medullary  matter  may  be  unduly  reddened.  The  large  joints 
contain  an  excess  of  synovia  of  a  somewhat  pinkish  color. 
The  ligaments  of  the  hip  joint  are  often  congested,  thickened 
and  softened.  The  articular  cartilages  may  even  show  areas 
of  blood  staining. 

The  intestines  are  usually  nearl}'  empty,  soft,  pale  and 
flaccid.  Ruthe  has  in  one  case  observed  rounded  ulcers  on 
the  mucosa. 

The  mesentery  is  thickened  with  an  infiltration  and  it  has 
a  yellowish  discoloration  and  the  mesenteric  glands  are  usually 
enlarged,  softened  and  friable,  though  .sometimes  firm  and 
contracted.  The  lymph  glands  adjoining  the  generative 
organs  are  often  swollen,  pigmented  and  studded  with  foci  of 
ca.seation,  varying  in  size  from  that  of  a  pea  upward.  The 
liver  is  softened,   hyperemic  or  fatt}-.      The  spleen  is    small. 


420  DOURINE 

The  kidneys  are  usually  large,  pale  and  blackened.  The 
thoracic  organs  may  show  little  change,  though  hypostatic 
congestions  and  foci  of  caseation  or  suppuration  may  be 
present.  The  blood  is  light  colored  and  forms  a  loose,  pale 
clot.  There  is  a  diminution  in  the  number  of  red  blood  cells 
and  a  relatively  large  increase  in  the  number  of  leucocytes. 

In  the  mare,  in  addition  to  the  lesions  in  the  internal 
organs  and  blood,  the  following  may  be  noted  in  connection 
with  the  generative  system.  Phlegmons  or  edematous  swell- 
ings, or  ulcers  on  the  lips  of  the  vulva  and  on  the  vulvar  and 
vaginal  mucosae.  The  parts  become  variously  distorted.  A 
crop  of  pu.stules  or  vesicles  which  run  into  ulcers  may  appear 
on  the  urethral  orifice,  the  vulva  and  adjacent  skin.  The 
mammary  glands  are  sometimes  inflamed,  edematous  and 
tender,  with  suppurative  or  necrotic  foci.  The  adjacent 
lymph  glands  are  enlarged  by  infiltration  or  contracted  by 
sclerosis. 

In  the  dog  the  symptoms  and  the  lesions  resemble  those 
in  the  horse. 

>^  323.  Differential  diagnosis.  Dourine  is  to  be  dif- 
ferentiated from  the  other  forms  of  Trypanosoma  disease,  and 
also  from  "  Benign  venereal  disease." 

Dourine  is  characterized  throughout  by  its  intermittence. 
As  each  fresh  crop  of  parasites  appears  in  their  cycle  of  exist- 
ence, there  is  an  exacerbation  of  symptoms,  but,  in  contra- 
distinction to  the  malarial  hematozoon  of  man  and  the 
piroplasma  of  cattle,  there  is  no  marked  rise  of  temperature 
and  a  correspondingly  low  fall. 

Williams  describes  a  benign  venereal  disease  of  mares  all 
of  which  had  been  bred  to  an  imported  French  draft  horse. 
He  states  that  "  the  margins  of  the  vulva  retain  their  natural 
color  in  this  disease,  except  at  the  seat  of  eruptions,  when  the 
color  quickly  returns.  The  vulva  remains  naturally  closed, 
and  does  not  gape, -as  in  maladie  du  co'it.  The  clitoris  retains 
its  natural  color,  size  and  appearance."  The  duration  of  this 
affection  is  stated  to  be  from  two  to  six  weeks,  but  may  persist 


PREVENTION  42  1 

for  a  longer  time  if  neglected.  The  cause  is  not  known.  He 
reports  that  when  it  becomes  established  it  is  highly  conta- 
gions.     It  appears  to  be  spread  by  copulation. 

>j  324.  Prevention.  The  prevention  of  this  disease 
seems  to  rest  in  the  isolation  of  all  affected  animals.  It  is 
important,  therefore,  that  its  diagnosis  be  made  at  the  earliest 
possible  moment.  As  it  is  not  spread  except  by  copulation,  it 
is  a  comparatively  easy  disease  to  control  if  taken  in  time. 

Prophylaxis. — In  Austria  where  the  disease  has  ex- 
isted for  a  long  time,  the  following  rules  are  observed" 
Baldrey  states  that  they  sum  up  the  necessary  preventive 
measures.  It  is  understood  that  they  apph'^  to  a  country  in 
which  the  disease  is  prevalent  : — 

"(i)  Even  when  there  is  nothing  to  lead  to  the  suppo- 
sition that  the  disease  exists,  everj-  mare  about  to  be  put  to 
the  horse  shall  be  carefully  inspected,  and  refusal  made  to  old 
and  weakly  mares,  or  to  those  which  have  a  discharge  from 
the  vulva,  or  have  that  organ  enlarged  or  swollen,  or  which 
do  not  present  the  ordinary  manifestations  of  oestrum.  It  is 
also  suggested  that  an  edematous  swelling,  no  matter  where 
situated,  should  negative  covering. 

"(2)  The  stallion's  penis  to  be  carefully  and  frequently 
examined,  and  on  no  account  is  the  animal  to  be  used  if  there 
is  the  slightest  lesion  upon  it.  He  is  to  be  kept  secluded  until 
all  doubt  as  to  the  nature  of  the  lesion  has  passed  away. 

"(3)  Give  every  information  possible  to  breeders  as  to 
character,  etc.,  of  the  disease. 

"(4)  Immediate  information  is  to  be  given  in  all  cases  of 
stallions  in  the  least  suspected,  and  the  necessary  steps  taken. 

"(5  )  To  prevent  extension,  the  sale  of  all  mares  in  the 
affected  areas  to  be  stopped  during  the  prevalence  of  the 
disease. 

"(6)  If  the  malady  has  spread  in  a  district,  all  breeding 
stallions  to  be  stopped  employment,  whether  Government  or 
private  property.     Those  already  diseased   to   be  sequestrated 


422  DOURINE 

under   police   supervision,    whether   private    or    Government 
property. 

"(7)  Affected  animals  to  be  separated  from  healthy,  to 
have  their  own  attendants,  and  no  interchange  of  clothing, 
utensils,  etc.,  to  take  place.  Those  deemed  curable  to  be 
treated,  those  incurable  to  be  destroyed. 

"(8)  All  horses  attacked  to  be  castrated,  as  well  as  those 
which,  notwithstanding  their  apparent  good  health,  have 
transmitted  it  to  mares  they  have  served,  and  also  those  which 
have  been  put  to  infected  mares. 

"(9)  Mares  that  have  been  in  the  least  affected  and 
apparently  cured  not  to  be  covered  the  following  year,  or  until 
certified  by  a  veterinary  surgeon  as  cured.  It  is  even  better 
to  exclude  all  such  mares  entirely,  and  brand  them  as  having 
had  the  disease." 

REFERENCES. 

1.  Baldrev.  Dourine.  Jour.  Coiiip.  Path,  and  T/wra.,  Vol. 
XVIII  (1905),  p.  I. 

2.  Buffard  and  Schneider.  Prophylaxie  de  la  douriue  et 
expose de  faits  nouveaux  interessant cette  maladie.  Jour,  de  Med.  I'et. 
et  de  Zoolch,  1901. 

3.  Faville.  Extirpation  of  maladie  dii  co'it.  Annual  Report, 
Bureau  oj Animal  Industry,  1895-6,  p.  13  and  62. 

4.  MoHLER.  Cultivation  of  Trypanosoma  Equiperdum.  Pro- 
ceedings Am.  Vet.  Med.  Asso.,  1905,  p.  363. 

5.  Rouf.ET.  Contribution  a  1'  etude  du  trypanosome  des  mammi- 
feres.     Amer.  de  V  Inst.  Pasteur,  \o\.  X  (  1896),  p.  716. 

6.  Thanhoffer.     tjber  Ziichilahme.     Wien.     18S8. 

7.  WiLi^iAMS.  Maladie-du-Coit,  or  equine  syphilis.  Annual 
Report  of  the  Board  of  Live  Stock  Commissioners,  for  the  State  of 
Illinois  Fiscal  Year  ending  Oct.  31,  1887.  (A  full  report  of  the  disease 
and  its  eradication  in  Illinois.) 

8.  Williams.  Benign  venereal  disease — equine  chancroid.  Ibid. 
p.  84. 

9.  Wilson-Barker.  Maladie  du  coit  in  Nebraska.  Vet.  four. 
Lond.,  Vol.  XXXV  (1892).     Vol.  XXXVI,  (1893). 


ETIOLOGY  423 

MAL  DE  CADKRAS 

§  325.  Characterization.  Mai  de  caderas  (disease  of 
the  rump)  is  a  disease  essentially  of  the  horse  kind,  charac- 
terized by  an  intermittent  fever,  a  progressive  paralysis  of  the 
posterior  parts,  rapid  emaciation  and  death.  It  is  a  "wet 
weather"  disease,  as  it  is  reported  to  almost  entirely  disappear 
in  the  dry  season.  Horses,  mules  and  asses  are  said  to  suffer 
from  it.      Horses  are  said  never  to  recover. 

§  326.  History.  Rebourgeon  studied  this  disease  in 
1889.  He  made  a  bacteriological  investigation  into  its  cause 
without  success.  Leclerc  described  it  clinically  in  1899.  He 
believed  that  he  had  found  its  pathogenic  bacterium.  In 
1 90 1,  Elmassian  showed  that  this  disease  was  caused  by  one 
of  the  trypanosoma.  Voges  and  Lignieres  confirmed  his 
discovery. 

§  327.  Geographical  Distribution.  Mai  de  caderas  i.= 
a  disease  of  tropical  South  America. 

§  328.  Etiology.  Elmassian  differentiated  the  try- 
panosoma of  this  affection  in  1901.  Voges  pointed  out  its 
pathogenic  action  and  named  it  Tr.  equinuvi.  In  length  it  is 
3  or  4  times  the  diameter  of  the  red  blood  corpuscles.  Its 
width  is  one-third  to  one-half  the  diameter  of  a  red  blood  cell. 

The  anterior  end  is  provided  with  a  flagellum  about  as 
long  as  the  body  of  the  parasite.  It  extends  backward  about 
two-thirds  the  length  of  the  body  as  a  somewhat  thickened 
margin  of  a  distinct  undulating  membrane.  The  posterior  end 
of  the  parasite  is  about  one-third  the  length  of  the  flagellum. 
It  is  contracted  and  somewhat  beak  shaped. 

Its  motion  resembles  that  of  an  eel,  but  its  actual  motility 
is  not  great,  the  whole  body  taking  part  in  an  excessively 
active  wriggling  motion  with  the  flagellum  and  beak  ends 
moving  in  opposite  directions.  The  nucleus  is  toward  the 
anterior  end,  a  very  small  centrosome  near  the  posterior  end, 
and  there  is  a  granular  protoplasm. 

It  is  found  in  the  blood  of  horses,  mules,  asses,    hogs  and 


424  MAL    DE    CADERAS 

water  hogs  suffering  from  mal  de  caderas.  It  is  transmissible 
to  white  and  gray  rats  and  mice,  rabbits,  dogs,  goats,  sheep, 
chickens,  turkeys,  ducks  and  certain  monkej^s  found  in  South 
America.     Cattle  are  said  to  be  immune. 

The  parasites  are  most  numerous  in  the  circulating  blood 
during  the  rise  of  temperature.  Upon  its  reaching  40-41°  C 
they  gradually  disappear,  but  reappear  with  the  next  rise  of 
temperature. 

^329.  Mode  of  infection.  Unlike  dourine,  the  virus  of 
mal  de  caderas  is  not  transmitted  by  copulation.  It  has  been 
proven  that  the  virus  is  disseminated  and  animals  are  infected 
with  it  by  means  of  certain  insects.  Stomoxys  calcitrayis  has 
been  incriminated  and  several  other  insects  are  under 
suspicion. 

4J  330,  Symptoms.  The  first  symptom  is  an  elevation 
of  temperature  which  rises  slowly,  but  suddenly  falls  to  nor- 
mal. Emaciation  is  rapid.  The  urine  is  dark  colored  and 
usually  contains  albumin,  and  perhaps  blood.  The  blood 
changes  so  that  it  gives  the  picture  on  microscopic  examina- 
tion of  pernicious  anemia.  There  is  an  increase  in  the  lym- 
phocytes and  in  the  eosinophiles.  The  most  obvious  symptom 
is  said  to  be  a  symmetrical  or  asymmetrical  paresis  of  the  hind 
legs.  Defecation  and  urination  are  difficult  (coinciding  with 
paralysis  of  the  sphincters).  The  paralysis  gradually  extends 
to  other  parts  of  the  body.  Edema  is  often  present.  The 
appetite  remains  good  until  near  the  end  when  there  is 
extreme  thirst. 

The  ditratioti  of  the  disease  is  variable.  Some  animals 
die  after  a  month,  others  live  for  a  year  or  longer.  Stiles 
states  that  it  lasts  from  two  to  five  months  in  horses  and  from 
six  to  twelve  months  in  mules  and  asses. 

?^  331.  Morbid  anatomy.  The  muscles  are  pale  and 
atrophied  in  the  posterior  part  of  the  body.  The  intermuscu- 
lar tissue  is  infiltrated  with  a  gelatinous  serous-like  substance. 
Hemorrhagic  foci  appear  in  the  muscles  of  the  rump. 


DIFFERENTIAL    DIAGNOSIS  425 

The  spleen  and  limphatic  glands  are  enlarged.  The  liver 
is  enlarged  and  congested.  The  heart  muscle  is  soft  and 
flabby.  The  lungs  often  contain  ecchymoses  and  subpleural 
emphysematous  areas.  There  is  a  serofibrinous  exudate  in  the 
body  cavities,  especially  in  the  pericardial  sac  and  pleural 
spaces.  There  are  conflicting  statements  concerning  the  mor- 
bid anatomy  and  it  is  difficult  to  select  those  that  are  not  con- 
tradicted. The  pathological  histology  and  the  lesions  in  the 
nervous  system  do  not  appear  to  have  been  described. 

i^  332.  Differential  diagnosis.  This  affection  is  to  be 
differentiated  from  the  other  forms  of  trypanosoma  infections. 
There  seems  to  be  no  other  specific  disease  with  which  it 
would  be  confused.  The  diagnosis  is  made  from  the  intermit- 
tent fever,  emaciation,  progressive  paresis,  anemia,  and  the 
finding  of  a  parasite.  The  inoculation  of  experimental  ani- 
mals (mice  or  dogs)  with  the  blood  is  of  value  when  the 
parasite  is  not  found  on  microscopic  examination  in  the  blood 
of  the  horse. 

REFERENCES. 

1.  Elmassian.  Mai  de  Caderas.  Analcs  de  la  Univcrsidad 
National  .Isniicioii,  Vol.  V  (1901). 

2.  I^ECLERC.     El  mal  de  Caderas.     Buenos  Ayres,  1899. 

3.  LiGNiiiRES.  Contribucion  al  estudio  de  la  trypanisomiasis  de 
los  Equideos  Sud  Americanos.  Buletin  de  agricultiira  y  yanaderia 
{Republic  Argentina)  1902,  p.  843. 

4.  RebourgEON.  Note  sur  le  mal  de  Cadera.  Recueil  de  mid. 
vHi'r.     1889,  p.  85. 

5.  SivORi  AND  LECLER.  Le  Surra  Americain  ou  mal  de  Caderas. 
Anales  del  ministerio  de  agricultura,  1902.  Centralbl.  fiir  allg.  Path. 
1902,  S.  963. 

6.  VOGES.  Uas  mal  de  Caderas.  Zeitschrifl  f.  Hygiene,  Bd. 
XXXIX   (1902),  p.  323. 

vSee  also  literature  011  other  trypanosoma. 


426  NAGANA 

NAGANA 

Synonym.     Tsetse-fly  disease. 

§  333-  Characterization.  Nagaua  is  a  disease  charac- 
terized by  anemia  and  rapid  emaciation  caused  by  one  of  the 
trypanosoma.  It  attacks  horses,  mules,  zebras,  cattle,  and 
sheep.  A  number  of  the  smaller  animals  are  susceptible.  It 
is  known  to  all  dialects  as  the  tsetse- fly  disease. 

§  334.  Geographical  distribution.  This  disease  is 
found  in  central  and  southern  parts  of  Africa.  There  seems 
to  be  some  doubt  about  its  identity  with  the  disease  of  a  simi- 
lar nature  in  the  Transvaal. 

§  335-  History.  Livingston  pointed  out  the  existence 
of  this  disease  in  Central  Africa.  In  1886,  Bruce  studied  it  in 
the  Zulu  Land.  He  found  constantly  in  the  blood  of  the  sick 
animals  a  trypanosoma  similar  to  that  found  in  surra.  It  has 
been  carefully  studied  by  Kanthack,  Durham  and  Blandford, 
Koel,  Plimmer  and  Bradford,  Theiler,  Schilling,  Laveian  and 
Mesnil. 

§  336.  Etiology.  This  affection  is  caused  by  Trypa- 
nosoma Brucei.  It  is  from  28  to  33  /<  in  length  with  the  flagel- 
lum  and  about  i  /<  in  width.  It  is  closely  related  to  Tr. 
equiperdiun.  Some  investigators  have  been  unable  to  satisfac- 
torily differentiate  the  two  species,  while  others  recognize  them 
as  distinct. 

The  trypanosoma  are  transmitted  from  the  diseased  to  the 
healthy  animals  by  means  of  the  tsetse-fly  {^Glosshia  )norsihi7is), 
which  exists  in  certain  parts  of  Africa.  It  appears  that  this  is 
the  only  species  of  insect  responsible  for  the  transmission  of 
the  virus.  The  affection  is  extended  into  uninfected  areas  by 
the  introduction  of  diseased  animals. 

The  pe7iod  of  incubation,  m  2ir\.\^c\a.\\Y  ■prod.nctd  cases,  is 
reported  to  be  about  4  days  in  the  horse. 

§  337-  Symptoms.  The  first  indication  of  the  disease 
is  a  rise  in  temperature  which  lasts  for  3  or    4    days,    when    it 


MORBID    ANATOMY  42? 

suddenly  drops.  After  this  time  the  temperature  oscillates 
between  35°  and  41  °  C.  Emaciation  is  rapid,  the  hair  becomes 
rouo-h  and  mav  fall  out.  There  is  a  tendency  to  diarrhea. 
There  is  edema  of  the  abdominal  walls.  In  cattle  the  symp- 
toms are  not  usually  so  acute  as  in  the  horse. 

The  duration  of  the  disease  is  said  to  vary  from  a  week  to 
six  months  or  more.  The  appetite  remains  good  until  near  the 
end.      According  to  Bruce  recovery  is  rare. 

^  338  Morbid  anatomy.  There  appear  to  be  no  dis- 
tinctive anatomical  changes  for  this  affection.  The  tissues 
generally  are  reported  to  be  anemic  and  infiltrated  with  a  ser- 
ous exudate.  If  the  edematous  portions  are  incised  a  clear 
amber  or  citron  colored  fluid  escapes.  The  spleen  may  be  en- 
larged but  the  color  and  consistency  are  normal.  The  liver 
and  kidneys  are  said  to  be  slightly  affected. 

S  339  Differential  diagnosis.  The  diagnosis  is  made 
clinically  from  the  progressive  anemia  and  edema,  coincident 
with  a  good  appetite.  The  finding  of  the  parasite  in  the  blood 
is  positive  evidence.  This  disease  is  to  be  differentiated  from 
the  other  affections  caused  by  trypanosoma. 

REFERENCES 
I.     BRrcE.     Preliminary  report  on  the  tsetse-fly  disease  or  nagaua. 

in  Zululand.     Durham,  1895.  ^ 

2  K^NTH^CK.  DURHAM  AND  Blandford.  On  nagana  or  tsetse- 
fly  iJ^  Proceedings  of  the  Royal  Society,  Vol.  LVIV  (X898) ,  P-xoo. 

,  L^VERAN  ANr>  MESNiL.  Recherches  morphologiques  et  exper- 
i^neniales  snr  le  trypanosome  dn  nagana  ou  maladie  de  la  mouche 
tsetse,     -inn.  de  F  lust.  Pasteur,  1902,  p.  i. 

4  PUMMER  AND  BR..DFORD.  A  preliminary  note  on  the  mor- 
phology and  distribution  of  the  organism  found  in  the  tsetse-fly  disease. 
The  Veterinarian,  Vol.  LXXII  ( 1899),  p.  64S. 

5.     TheilER.     Die  Tsetse-Krankheit.    Schz.cizer-Archiv  n<r  Thter- 

heill:.,  1901.  S.  97. 

^  340       Differentiation    of    surra,     dourine,     mal    de 
caderas   and   nagana.     The  divergence  of  opinion  concern- 


428  TRYPANO.SO:\IIASES 

ing  the  nature  of  these  affections  and  the  specific  identity  of 
the  exciting  cause,  render  a  dififerentiation  or  unification  of 
these  most  interesting  diseases  exceedingly  difficult.  Very 
few  investigators  have  had  the  opportunity  of  studying  all  of 
them  in  their  natural  environment.  The  conclusion  of  Mus- 
grave  and  Clegg  in  their  recent  report  is  worthy  of  considera- 
tion. They  say:  "In  summing  up  the  whole  matter  it 
appears  to  us,  when  we  take  into  consideration  the  work  done 
by  others  and  add  our  own  results,  that  we  are  justified  in 
believing  surra,  nagana,  mal  de  caderas,  and  probably  dourine, 
the  same  disease,  and  that  all  are  caused  by  Tr.  Evansii." 

Koch,  who  worked  with  surra  and  nagana,  considered 
the  parasites  and  the  resulting  infections  identical.  Many 
others  have  formed  similar  conclusions.  Other  investigators 
such  as  Voges,  Laveran  and  Mesnil  and  others  maintain  that 
certain  differences  exist.  The  evidence  is  convincing  that 
dourine  and  mal  de  caderas  are  different  in  some  respects  from 
the  other  two.     Voges'  reasons  for  this  are  : 

1.  "Dourine  and  mal  de  caderas  can  not  be  transmitted 
to  cattle. 

2.  "In  regions  where  mal  de  caderas  exists  cattle  do  not 
die  of  surra. 

3.  "We  Jiave  no  reason  to  believe  that  trypanosoma 
show  the  same  irregularities  of  virulence  as  bacteria,  so  that 
the  different  forms  of  the  disease  may  be  said  to  be  produced 
by  different  degrees  of  virulence  in  the  same  trypanosoma. 
On  the  contrary,  during  our  four  years  of  experimentations, 
the  latter  have  .shown  a  constant  virulence." 

4.  The  fourth  reason  which  he  considers  decisive  is 
based  on  the  morphological  differences  in  the  parasites. 

Voges  concludes  by  saying,  "I  think  these  four  proofs  are 
entirely  sufficient  to  establish  for  all  time  the  difference  be- 
tween surra  and  dourine  as  well  as  between  surra  and  )nal  de 
caderas. ' '  I^averan  and  Mesnil  give  extensive  consideration  to 
the  differences  between  surra  and  nagana.  A  summary  of 
their  considerations  is  appended. 


DIFFERENTIATION  429 

1.  "The  same  animals  are  susceptible  to  both  diseases — 
the  horse,  ass,  mule,  goat,  sheep,  cow,  camel,  dog,  cat, 
monkey  (long-tailed  macayo),  rabbit,  guinea-pig,  and  rat. 

2.  "In  the  horse  the  course  of  the  disease  is  the  same, 
whether  surra  or  nagana.  The  animal  dies  at  the  same  time, 
in  30  days  on  the  average.  In  inoculation  cases  the  period  of 
incubation  is  the  same,  and  the  same  symptoms  and  lesions 
supervene. 

3.  "The  other  equides,  the  goat,  sheep  and  dog,  die  of 
the  two  diseases  in  the  same  length  of  time  and  with  similar 
.S3'mptoms  and  lesions. 

4.  "Rabbits,  guinea-pigs  and  rats  succumb  to  the  infec- 
tion in  a  like  manner. 

5.  "Cows  rarely  survive  naga)ia,  and  they  rarely  die 
from  surra.  They  become  emaciated  with  surra  but  recover 
in  health  and  a  subsequent  inoculation  does  no  harm.  This  is 
a  marked  difference  between  them  but  it  may  be  explained 
when  further  experiments  are  made." 

Laveran  and  Alesnil  believe  that  the  paralysis  of  the  pos- 
terior extremities,  a  marked  symptom  in  mal  de  cad  eras,  is  less 
marked  in  surra  and  nagana,  although  they  believe  the  three 
affections  verj'  closely  related.  Dourine  differs  from  the  other 
three  in  two  distinct  points  :  ( i )  The  morphology  of  the  para- 
site is  different.  {2)  In  dourine  contagion  by  coition  seems 
to  be  the  only  natural  mode  of  infection. 

Much  additional  investigation  will  be  necessary  before 
the  question  of  either  the  identity  or  the  non-identity  of  these 
affections  can  be  positively  determined.  As  these  diseases 
are  not  liable  to  become  of  great  economic  importance  in  this 
country,  further  discussion  of  the  voluminous  literature  seems 
unnecessarv. 


CHAPTER  XII. 

INFECTIOUS  DISEASES  FOR  WHICH  THE  SPECIFIC 
CAUSE  IS  NOT  DETERMINED. 


§  341.  General  consideration.  It  was  not  until  a 
comparatively  recent  date  that  the  nature  of  the  infectious 
diseases  began  to  be  understood.  The}'  were,  however,  differ- 
entiated in  so  far  as  that  could  be  done  by  clinical  evidence 
alone.  With  the  work  of  Pasteur,  overthrowing  the  "spon- 
taneous generation"  theory;  the  introduction  of  the  aniline 
dyes  by  Weigert  in  1877  i  the  discovery  of  solid  culture  media 
by  Koch  in  1881  ;  together  with  the  finding  of  the  specific 
causes  of  anthrax,  Asiatic  cholera,  tuberculosis  and  other  dis- 
eases, there  naturally  came  new  methods  for  the  study  of  the 
etiology  of  these  affections.  By  the  use  of  newer  methods 
and  better  instruments  of  precision  and  the  closer  study  of. 
these  afifections  the  cause  of  one  after  another  of  the  infectious 
diseases  was  revealed  until  the  etiology  of  a  large  number  of 
them  has  been  made  known.  These  have  already  been  grouped 
and  studied.  There  are  remaining  still  a  number  of  well 
recognized  diseases  for  which  a  specific  cause  has  not  been 
found.  The  methods  for  the  investigation  of  the  cause  of  dis- 
ease that  have  been  effective  in  case  of  other  diseases  have 
failed  here.  Until  other  procedures  are  devised,  the  specific 
causes  of  these  affections  will  undoubtedly  remain  undeter- 
mined. Their  study,  however,  has  revealed  much  concerning 
their  nature,  so  that  measures  for  their  prevention  have  been 
found  that  are  quite  as  effective  as  they  are  with  those  of 
known  etiology. 

RINDERPEST. 

Syno7iy7ns.     Contagious  typhus  ;   steppe  murrain  ;    cattle 
plague. 


HISTORY  431 

§  342.  Characterization.  Rinderpest  is  the  most  fatal 
disease  affecting  cattle.  It  is  a  specific  eruptive  fever,  occur- 
ring both  sporadically  and  in  epizootics.  It  is  characterized  by 
a  more  or  less  typhoid  condition,  with  lesions  largely  located 
in  the  mucosa  of  the  digestive  tract  and  skin,  and  by  the  in- 
fectious nature  of  all  the  tissues,  secreta  and  excreta.  It  is  a 
disease  peculiar  to  cattle,  although  other  ruminants  are  sus- 
ceptible to  it. 

^  343.  History.  Rinderpest  seems  to  have  been  brought 
to  western  Europe  by  the  importation  of  cattle  from  central 
Asia  as  early  as  the  fourth  century.  It  is  supposed  that  it 
had  long  existed  on  the  steppes  of  central  Asia  and  eastern 
Europe  The  first  great  epizootic  of  which  there  seems  to  be 
records  occurred  about  1709  and  spread  over  nearly  all  of  the 
countries  of  Europe.  It  is  reported  that  1,500,000  cattle  died 
from  its  effects  during  the  years  from  1711  to  1714-  Ramaz- 
zini  seems  to  have  been  the  first  (1711)  to  accurately  describe 
the  symptoms  and  lesions. 

It  was  in  connection  with  this  disease  that  the  first  veteri- 
nary  police  regulations   were  instituted,  and  it  is  stated  that 
because  of  the  ravages  of  this  affection  Veterinary  Colleges 
were  first  established  with  government  aid.     In  the  latter  half 
of  the  eighteenth  century,  rinderpest  was  prevalent  in  nearly 
all  of  the  countries  of  Europe.     During  the   years   from    1740 
to   1750  it  was  estimated  that  three  million  cattle  died.     The 
importance  of  this  disease  is  shown  in  the  fact  that  m  Italy 
alone  during  the  year  1792  from   three  to  four  million  cattle 
died  from  its  effects.      In  the  years  1844  and   1845,  Russia  is 
said  to  have  lost  a  million  of  cattle  from  this  disease  alone. 
Nearly  all  the  countries  of  Europe  have  from  time  to  time  lost 
heavily  from  it.     It  is  stated,  however,  that  England  and  Ger- 
many have  practically   freed  themselves  from  it.     Preventive 
inoculation   against  this  disease  was  introduced  into  England 
by  Dodson  as  early  as  1744  and  later  by  Courtivon  into  France. 
§  344      Geographical    distribution.       Rinderpest    is   a 
well-known  cattle  plague  in  Russia  and  the  steppes  of  central 


432  RINDERPEST    . 

Asia.  It  has  extended  from  time  to  time  from  its  home  in 
Russia  and  Asia  to  nearlj^  every  countr}-  in  Continental 
Europe  and  Asia.  More  recently  it  has  occurred  in  southern 
Africa.  In  1882/'^  it  appears  to  have  been  introduced  into  the 
Philippines.  It  has  not  been  introduced  into  the  United  States 
or  other  American  countries.  At  present,  it  is  not  known  to 
exist  in  England,  although  in  the  past  she  has  suffered  many 
destructive  epizootics. 

s^  345.  Etiology.  The  specific  etiological  factor  of  rin- 
derpest is  not  known.  vSeveral  investigators  have  isolated  and 
studied  various  species  of  bacteria  from  the  tissues  of  animals 
dead  from  this  disease.  Semmer  of  Dorpat  has  always  found 
the  same  organism  in  the  lesions.  His  results  do  not  appear 
to  have  been  verified.  There  seems  to  be  no  doubt  in  the 
minds  of  those  who  have  worked  on  this  disease  that  it  is 
caused  by  a  specific  microorganism,  most  likely  a  species  of 
bacteria.  Koch  makes  the  following  statement  concerning  the 
etiology  of  rinderpest  in  the  second  report  of  his  investigations 
in  South  Africa  in  1897  :  "  All  efforts  to  find  by  means  of  the 
microscope,  as  well  as  through  cultivation,  a  specific  micro- 
organism in  the  blood  have  as  yet  been  fruitless.  I  also  did 
not  succeed  in  finding  any  specific  microorganism  amongst  the 
microbes  which  the  mucus  from  the  nose,  the  secretions  from 
mucous  membranes,  and  the  contents  of  the  intestines  natur- 
ally contain  in  large  numbers."  Jobling  reports  that  o.i  cc. 
of  blood  taken  from  a  sick  animal  and  injected  under  the  skin 
of  a  healthy  one  will  produce  the  disease. 

NicoU  and  Adil-Bey  found  that  the  virus  would  usually 
pass  through  the  porous  Berkfeld  cylinders,  but  not  through 
the  denser  form  or  the  Chamberland  tube. 

The  virus  may  be  transmitted  from  the  sick  to  the  healthy 
individuals  in  a  variety  of  ways,  both  direct  and  indirect.  It  is 
said  to  be  present  in  the  various  excreta  of  the  diseased  animal, 
such  as  the  discharge  from  the  nose,  the  saliva,  the  urine  and 


*No   authoritative   evidence   of  its   occurrence  there  prior  to  that 
time  has  been  found. 


SYMPTOMS  433 

the  feces.  It  retains  its  vitality  outside  of  the  body  in  a  moist 
state  for  months,  even  a  year  or  more,  according  to  some  au- 
thorities. Hence,  feces  and  the  fodder  and  bedding  soiled  by 
the  discharges  may  convey  the  disease.  When  dried,  how- 
ever, its  vitality  is  said  to  be  lost  in  a  few  days.  Persons  may 
carry  the  virus  on  their  shoes,  clothing  and  farm  implements. 
Even  small  animals  such  as  cats  and  rats,  which  frequent 
barns  and  stables,  have  been  looked  upon  as  carriers  of  the 
infection.  The  hides  of  animals  dead  of  the  disease  may  trans- 
mit the  infection.  The  virus  is  destroyed,  according  to  Hutch- 
eon,  by  complete  desiccation.  Kraiewsky  found  that  the  virus 
was  destroyed  in  hides  soaked  in  corrosive  sublimate  i-iooo 
for  24  hours,  or  in  2.4  per  cent  carbolic  acid  for  the  same  time. 
It  is  also  claimed  that  animals  after  having  pas.sed  through 
one  attack  of  the  disease  are  able  to  resist  successfully  future 
attacks.  Inoculation  with  the  virus  is  said  to  produce  immun- 
ity, but  the  process  of  inoculation  itself  is  followed  by  death  in 
many  cases.  The  disease  is  reported  to  have  developed  after 
feeding  hay  a  year  after  it  has  lain  in  an  infected  stable.  It  is 
destroyed  at  a  temperature  of  131°  F.  but  in  animal  ti-ssues  it 
is  said  by  some  to  resist  putrefaction.  Hutcheon,  however, 
states  that  putrefaction  appears  to  destroy  it. 

The  period  of  mciibation  is  stated  to  be  from  three  to  ten 
days.  In  animals  inoculated  with  virulent  blood  it  is  from 
sixty  to  ninety- six  hours. 

§  346.  Symptoms.  The  symptoms  of  rinderpest  are 
those  of  a  severe,  acute,  infectious  disease.  At  first  the  tem- 
perature rises  to  105  to  106°  F.  and  remains  near  that  point 
with  but  slight  variations  until  other  symptoms  develop.  The 
pulse  is  small,  beating  from  160  to  120  per  minute.  There  is 
great  debility,  decrease  in  the  yield  of  milk  and  loss  of 
appetite  ;  rumination  becomes  disturbed  and  the  animal  may 
have  slight  attacks  of  shivering. 

After  these  preliminary  symptoms  there  are  well  marked 
rigors,  respiration  becomes  accelerated  and  the  visible  mucous 
membranes  assume  a  scarlet  color.     There    is    entire    loss   of 


434  RINDERPEST 

appetite,  arrest  of  the  function  of  rumination,  thirst,  consti- 
pation with  the  feces  dry  and  covered  with  mucus.  Some- 
times there  is  slight  colic.  Later  there  is  a  discharge  which 
is  first  serous  and  subsequently  sero-raucous  from  the  eyes, 
nose  and  vagina.  The  saliva  flows  from  the  mouth.  The 
feces  gradually  become  thinner  until  violent  diarrhea  accom- 
panied by  colic  sets  in.  The  evacuations  become  fetid,  viscid 
and  sometimes  mixed  with  blood.  The  animal  becomes  rapidly 
emaciated,  staggers  when  w^alking,  is  very  sensitive  to  pressure 
on  the  loins  and  lies  down  a  great  deal.  In  exceptional  cases 
the  patient  manifests  nervous  symptoms.  Others  exhibit  vio- 
lent dyspnea  and  symptoms  of  severe  inflammation  of  the  lungs. 

As  the  disease  advances  characteristic  changes  are  to  be 
seen  in  the  mucous  membranes.  Red  patches  which  may  be 
flat  or  in  the  form  of  wheals  and  which  quickly  become  cov- 
ered with  a  grayish  white,  loose  crust  appear  on  the  mucous 
membrane  of  the  lips,  tongue,  cheeks,  gums,  nostrils  and 
vagina.  The  uppermost  epithelial  layer  consequently  becomes 
opaque  and  yellowish  gray  spots  develop  on  it.  Less  frequently 
crusts  are  formed  from  the  tumors  bj-  their  caseous  disintegra- 
tion. The  crusts  on  being  shed  leave  dark  red  hollow  places, 
the  so-called  erosion  ulcers,  which  readily  bleed.  In  slight 
cases  of  the  disease  there  may  be  no  crusts  or  erosions.  It  is 
stated  that  sometimes  an  eruption  in  the  form  of  very  minute 
pimples  and  pustules  occurs  on  the  abdomen,  inner  surface  of 
the  thighs,  perineum  and  udder.  In  these  cases  it  may  be  con- 
fused with  that  of  variola.    Pregnant  animals  frequently  abort. 

In  sheep  and  goats  the  disease  is  milder,  and  its  infec- 
tiousness is  said  to  be  less  than  in  cattle,  although  the  symp- 
toms are  essentially  the  same.  Sheep  are  reported  to  suffer 
frequently  from  pneumonic  affections  when  attacked  by 
rinderpest. 

§  347.  Morbid  anatomy.  Authors  differ  somewhat  on 
the  lesions  characteristic  of  this  disease.  Walley  has  pointed 
out  the  fact  that  none  of  the  morbid  changes  are  constant  and 
consequently   they   vary  with  the  stages  of  the  epizootic,  the 


MOKBII)    AXATO>rV  435 

condition  of  the  animal  and  the  treatment.  There  is  always 
emaciation,  the  muscular  tissue  is  dark  and  the  capillary  con- 
gestion is  marked.  All  the  tissues  of  the  body  may  be  the 
seat  of  effusions,  exudations  and  blood  extravasations.  If 
symptoms  referable  to  the  nervous  system  have  occurred, 
brain  lesions  will  be  found  at  post-mortem. 

The  muscle  of  the  heart  is  pale  and  relaxed.  Blood  extra- 
vasations beneath  the  endocardium  are  not  rare.  The  kidneys 
are  usually  the  seat  of  congestion  or  ecchymoses  either  beneath 
the  capsule  or  in  their  structure.  There  are  also  parenchyma- 
tous changes.  The  liver  is  congested,  often  giving  a  mottled 
appearance.  It  is  often  bile  stained.  There  are  more  or  less 
parenchymatous  changes  in  the  liver  cells.  The  lymphatic 
glands  are  usually  enlarged  and  the  mesenteric  glands  are 
often  hyperemic  or  even  hemorrhagic. 

The  structures  most  often  affected  are  the  mucous  mem- 
branes of  the  digestive,  respiratory  and  genito- urinary  tracts 
and  the  skin. 

Nodules  and  pustules  are  sometimes  found  on  the  skin, 
especially  of  the  udder.  The  mucous  membrane  of  the  mouth 
and  pharynx  is  congested  in  spots,  swollen  and  exhibits 
rounded,  yellowish  gray,  caseous  plates  or  deposits.  The 
removal  of  plates  discloses  ulcerous  and  highly  congested 
depressions  in  the  mucous  membrane,  the  so-called  erosion 
ulcers.  These  changes  are  best  marked  on  the  inner  surface 
of  the  lips,  lower  surface  of  the  tongue,  buccal  mucous  mem- 
brane and  gums  of  the  inferior  maxilla. 

In  the  first  three  stomachs  the  mucous  membrane  is  usu- 
ally normal  or  slightly  congested  in  spots,  and  the  epithelium 
is  so  loose  that  it  can  be  easily  detached.  The  contents  of  the 
rumen  and  reticulum  are  soft  and  those  of  the  omasum  are 
often  dried,  rarely  they  are  fluid.  Generally  the  abomasum 
is  empty  and  contains  only  a  small  quantity  of  tough,  muco- 
purulent, yellow  or  sanious  material.  Its  mucous  membrane 
is  highly  congested,  especially  in  the  neighborhood  of  the 
pyloric  orifice.  The  congestion  is  partly  diffuse,  partly  in 
spots,    in    the    form    of   points   or    streaks.      Its  color  may  be 


436  RINDERPEST 

purple  or  reddish-brown  with  a  tinge  of  slate-gray.  The 
epithelium  exfoliates.  On  the  mucous  membrane  may  be 
found  small,  brownish-yellow,  caseous  deposits,  in  the  form  of 
plates,  which  become  detached  in  shreds,  leaving  indented, 
highly  reddened  areas  which  are  studded  with  petechiae.  The 
glands  (peptic  and  mucous)  of  the  stomach  are  .swollen  and 
show  considerable  cellular  hypertrophy.  Like  changes  are 
present  in  the  small  intestine,  where  there  is  a  good  deal  of 
swelling  and  congestion  of  the  mucous  membrane  with  isolated 
scab-like  caseous  deposits  and  erosions.  In  very  severe  cases 
these  deposits  form  tube-like  casts  of  the  intestinal  canal.  At 
the  same  time  there  may  be  considerable  infiltration  of  the  soli- 
tary glands  and  of  Peyer's  patches,  which  become  enlarged. 
Jobling  states  that  he  never  saw  them  ulcerated. 

In  the  large  intestine  the  inflammatory  changes  are  much 
less  pronounced.     They  are  greatest  in  the  cecum. 

The  nasal  mucous  membrane  is  of  a  dark  red  color  and 
covered  with  grayish-yellow,  soft  scabs.  After  they  are  re- 
moved, the  true  tissue  of  the  mucous  membrane  lies  bare. 
Similar  changes  are  found  in  the  larynx  and  trachea,  where 
the  deposited  masses  are  frequently  purulent  and  of  a  creamy 
consistence.  The  lungs  are  sometimes  hyperemic,  sometimes 
edematous,  hepatised  or  emphysematous.  Pneumothorax  and 
subcutaneous  emphysema  may  be  present. 

The  duration  of  the  disease  is  usually  from  2  to  lo  days, 
the  average  period  is  about  6  days.  The  prognosis  is  not 
favorable.     The  mortality  ranges  from  60  to  90  per  cent. 

§  348.  Differential  diagnosis.  It  is  very  difficult  to 
diagnose  rinderpest  from  the  first  cases  that  occur,  especially  if 
there  is  no  history  of  infection.  The  diagnosis  is  based  upon 
the  symptoms,  morbid  anatomy,  progress  of  the  epizootic  and 
the  history.  The  most  characteristic  diagnostic  symptoms  are 
the  rise  in  temperature  (which  often  occurs  some  days  before 
other  symptoms),  formation  of  red  spots  and  a  yellow  coating 
on  the  visible  mucous  membranes  and  later  the  development 
of  erosion  ulcers.  A  mucous  discharge  from  the  mouth,  nares, 
eyes  and  vagina  with  symptoms  of  severe  intestinal  disturb- 


PRKVENTION' 


437 


ances  and  excessive  emaciation  are  of  differential  value. 
Rinderpest  is  to  be  differentiated  from  "  foot  and  mouth 
disease,"  and  malignant  catarrh  if  complicated  with  emph\- 
sema  of  the  lungs.  Anthrax,  Texas  fever,  and  other  affections 
such  as  contagious  pleuropneumonia  and  enteritis  may  be  mis- 
taken for  it.  The  differentiation  may  be  made  from  the  specific 
nature  of  eacii  disease. 

s^  349.  Prevention.  In  this  connection  the  proclama- 
tion for  the  prevention  of  the  spread  of  rinderpest  in  Cape 
Colony  recently  issued  by  the  British  Government  authorities 
is  of  interest.      It  is  as  follows  : 

"Disinfection  of  hides,  /loo/s,  horns,  skins  and  feathers,  i.  Hides 
skins,  hoofs,  horns  and  feathers  will  only  be  allowed  south  of  Orange 
River  and  will  onl}'  be  accepted  for  conve3^anGe  by  rail  after  being 
thoroughly  disinfected  in  the  manner  hereafter  described  at  railway 
stations  and  the  authorized  crossing  places  in  terms  of  Regulation  5 
issued  under  Proclamation  No.  387  of  1896,  or  at  each  of  them  as  shall 
hereafter  be  notified. 

2.  No  hides,  skins,  horns  or  hoofs  shall  be  passed  by  the  Supervis- 
ing Officer  unless  accompanied  by  a  declaration  signed  V)y  the  consignor 
(or  his  agent)  that  they  are  from  animals  that  have  not  died  from  rinder- 
pest. Any  hides,  skins,  horns  or  hoofs  not  accompanied  by  such  declar- 
ation, shall  be  immediately  destroyed  by  the  Supervising  Officer  at  the 
consignor's  expense. 

3.  Disinfection  shall  be  supervised  by  the  officer  appointed  by  the 
Government  for  the  purpose,  but  shall  be  performed  by  the  owners  or 
consignors  or  their  agents. 

4.  Dried  hides,  horns  or  hoofs  shall  be  immersed  in  a  li(|uid  disin- 
fectant for  at  least  30  minutes. 

5.  (ireen  hides  and  skins  shall  be  immersed  in  a  liciuid  disinfectant 
for  a  period  of  at  least  15  minutes. 

b.  The  disinfectant  used  may  be  either  a  two  per  cent  solution  of 
carbolic  acid  or  a  five  per  cent  solution  of  Jaye's  Disinfectant,  Odam's 
Disinfectant  or  I/.al. 

7.  Feathers  shall  be  hung  up  for  three  hours  in  a  chamber  charged 
with  sulphurous  acid  produced  by  burning  an  excess  of  sulphur  in  a 
closed  chamber. 

8.  Hides,  skins,  horns,  hoofs  and  the  packages  containing  feathers 
when  disinfected,  shall  be  marked  for  the  guidance  of  the  railway  offi- 
cials, and  shall  l)e   accompanied   by  a  certificate  that   disinfection   has 


438  RINDERPEST 

been  efficiently  performed,  signed  bj^  the  supervising  oi^cer  without 
which  the  railwaj'  officials  shall  refuse  to  receive  the  articles. 

9.  When  disinfection  is  completed,  the  articles  disinfected  shall  be 
loaded  direct  into  a  previously  disinfected  railway  truck. 

10.  Drying,  salting  or  any  other  subsequent  treatment  of  the  hides 
or  skins  shall  be  done  by  the  owners  or  their  agents  at  their  own  risk." 

"Disinfection  0/  travelers  or  passengers.  1.  Travelers  and  passen- 
gers shall  be  disinfected  at  railway  stations  and  at  authorized  crossing 
places,  in  terms  of  Regulations  7  and  8  issued  under  Proclamation  No. 
587  of  1896,  by  the  police  or  other  persons  duly  authorized  by  the  Sec- 
retary of  Agriculture  in  the  manner  hereafter  described. 

2.  Natives  shall  strip  and  enter  a  bath  containing  2  per  cent  solu- 
tion of  carbolic  acid;  they  shall  then  be  provided  with  a  blanket  or 
other  suitable  clothing  until  the  clothes  they  are  wearing  have  been 
disinfected. 

3.  The  clothing  of  all  natives,  and  the  blanket?,  rugs,  karrosses, 
wraps,  etc.,  of  all  Europeans,  whether  from  disinfected  areas  or  not, 
shall  be  subjected  to  sulphurous  acid  fumes  produced  by  burning  an 
excess  of  sulphur  in  a  closed  chamber  for  at  least  15  minutes,  pending 
arrival  and  erection  of  a  proper  steam  disinfecting  apparatus. 

4.  Europeans  coming  from  an  infected  farm  or  place  or  who  have 
otherwise  rendered  themselves  liable  to  infection  from  contact  with 
natives  or  their  huts  or  kraals,  shall  be  disinfected  in  such  a  manner  as, 
in  the  discretion  of  the  disinfecting  officer,  may  be  deemed  necessary 
and  their  clothing  as  provided  by  clause  3. 

5.  The  disinfectant  to  be  used  shall  be 

2  per  cent  solution  of  carbolic  acid  or 

5  per  cent  solution  of  Jaye's  Fluid  or 

5  per  cent  solution  of  Odam's  Disinfectant  or 

5  per  cent  solution  of  Izal. 

6.  Boots  of  Europeans  and  natives  shall  be  well  dry  brushed,  and 
then  the  uppers  and  soles  well  wiped  with  the  disinfecting  solution  by 
means  of  cloths. 

7.  Europeans  on  coming  from  an  infected  farm  or  place  and  all 
natives  presenting  themselves  at  a  railway  station,  siding,  halt  or  other 
place  north  of  the  Orange  River,  shall,  before  the  station  master,  clerk, 
guard  or  other  officer  permits  them  to  obtain  a  traveling  ticket,  hand  to 
the  station  master  or  booking  clerk  a  certificate  signed  by  the  disinfect- 
ing officer  in  terms  of  Form  A,  to  the  effect  that  they  and  their  clothes 
have  been  properly  disinfected  as  well  as  such  articles  and  things  in 
their  possession  as  are  intended  to  be  carried  by  rail,  not  being  articles 
or  things  actually  prohibited  to  be  carried  south  of  the  Orange  River. 


niMUNIZIXG 


439 


8.  Any  European  not  coming  from  an  infected  farm  or  place  or 
who  has  not  in  any  way  been  liable  to  infection,  shall  si.<<n  a  certificate 
to  that  effect  in  terms  of  Form  B,  and  without  such  certificate  shall  be 
deemed  as  coming  from  an  infected  farm  or  place,  or  otherwise  been 
liable  to  infection,  and  shall  be  subject  to  all  provisions  and  regulations 
attached  to  persons  coming  from  infected  areas  or  liable  to  infection  ; 
and  if  the  above  certificate  contains  any  false  statement,  the  person 
signing  the  same  will  be  liable  to  a  penalty  not  exceeding  loo  pounds 
or,  in  default  of  payment,  to  imprisonment  with  or  without  hard  labor, 
for  a  period  not  exceeding  six  months." 

Riudcrpcst 


This  is  to  certify  that together  with  his 

clothes  and  the  articles  or  things  in  his  possession,  authorized  to  be  car- 
ried by  rail,  have  been  properly  disinfected  as  required  by  the  Govern- 
ment Regulations, 

Disinfecting  Officer. 
Riyiderpest. 
FORM     B. 

I of do  hereby 

certify- that  I  have  not  come  from  any  farm  or  place  infected  with  rin- 
derpest, and  I  have  not  in  any  way,  to  the  best  of  my  knowledge  and 
belief,  come  in  contact  with  infection. 

(Signed). 

^  350.  Immunizing  cattle.  Koel  found  that  the 
serum  of  an  aniinal  that  had  suffered  from  rinderpest  and 
recovered  possessed  immunizing  powers.  This  fact  being 
demonstrated,  its  utility  has  been  availed  of  in  immunizing 
animals  for  procuring  the  serum.  The  method  given  by 
Jobling  and  which  is  u.sed  extensively  in  the  Philippines  is 
appended. 

The  animal  first  receives  an  inoculation  by  the  "simulta- 
neous method"  of  Kolle  and  Turner.  This  consists  in  inject- 
ing under  the  skin  on  one  side  from  15  to  55  cc.  of  .serum 
from  an  immune  animal  and  on  the  other  side  i  cc.  of  virulent 
blood  from  a  sick  animal.  If  the  reaction  from  this  double 
injection  is  good,  i.  e.,  a  rise  of  temperature  after  the  proper 
period,  it  is  given  1000  cc.  of  virulent  blood  after  the  tempera- 


440  RINDERPEST 

ture  again  drops  to  normal.  This  is  followed,  under  the  same 
circumstances,  by  500  cc.  and  again  1000  cc.  After  this  the 
animal  is  bled  for  serum.  They  are  bled  with  a  trocar  and 
canula  from  the  jugular  vein.  The  animals  are  bled  three 
times  at  intervals  of  a  week,  after  which  they  are  injected 
again  with  1000  cc.  of  virulent  blood. 

In  using  the  serum  from  50  to  100  cc.  should  be  injected 
subcutaneously  by  aseptic  methods. 

The  advantages  of  this  method  of  immunizing  cattle  are  : 
(i)  It  produces  no  reaction,  (2)  it  does  not  check  the  flow  of 
milk,  (3)  it  confers  immunity  almost  immediately,  (4)  if 
the  disease  has  just  begun  it  will  modify  the  attack  resulting 
in  a  milder  form,  (5)  no  deaths  follow  its  use,  (6)  pregnant 
animals  do  not  abort,  and  (7)  the  serum  can  be  prepared  in 
any  quantity  and  it  can  be  kept  for  seven  or  eight  months. 

The  disadvantages  of  this  method  are  ( i )  the  short  period 
of  immunity — 2  to  4  months,  (2)  skill  required  to  obtain  the 
serum,  (3)  occasionally,  according  to  Jobling,  very  little 
immunit\'  is  conferred. 

The  other  methods  that  have  been  tried  with  more  or  less 
success  are  :  inoculation  with  attenuated  virus  ;  injection  of 
the  bile  of  animals  dead  of  the  disease  ;  injecting  the  bile 
associated  with  virulent  liquid  ;  the  injection  of  the  serum 
from  immune  animals. 

REFERENCES. 

1.  Danvs/.,  Brodet  Axn  Theiler.  The  /  V/.  /onrnal.  \o\. 
XLVI  (1898),  p.  298. 

2.  EdingTox.  Report  of  investigation.  T/ir  Veieriiiary  Journal, 
Vol.  XLVI  (189S),  p.  64. 

3.  G.wigee.     The  cattle  plague.     London.     1866. 

4.  Holmes.  vSome  diseases  complicating  rinderpest  among  cattle 
in  India.    Jour.  Comp.  Path,  and  Thera.,  Vol.  XVII  (1904),  p.  317. 

5.  JoBUNG.  Report  of  the  Director  of  the  Serum  Laboratory. 
Fourth  annual  report  oj the  Philippine  Islands.  1903.  Ibid.  Bulletin 
No.  7,  Bureau  of  Governtnetit  Laboratories.     Manila,  igo^. 

6.  Koch.  Report.  The  Veterinary  Journal,  \'ol.  XLV  (1897), 
p.  204.     Wso  Centralblf.  Bakteriol.     Bd.  XXI  (1897),  S.  526. 


CONTAGIOUS    PLEURO-l'NKUMONIA  44^ 

-  KoLiE  IND  Turner.  Uber  SchutzimpfmiKen  und  Heilseruti. 
bei  Rinderpest.     Zeit.  f.  Hygiene,  Bd.  XXIX  (.898),  S.  309- 

8.  Ram.'^/./-INI.     Dissertatio  de  Contagiosa  Epidemica,  Padua,  1711. 

9.  TiRNEK  AND  K01.LK.  Report  of  investiKations.  The  Vet. 
lour.     Vol.  XLV  (1897),  p.  462. 

10.  Wai.t.kv.     The  four  bovine  scovirges.     London.      i.S79- 

1  ■  Wai  kkr  The  prophylactic  treatment  of  rinderpest  by  means 
of  preventive  hiocnlations,  more  especially  considered  i"  regard  to  the 
conditions  prevailing  in   India.    Jour.    Con.p.   Path,  and   fhera.,   \o\. 

XVII  (1904),  P-  326. 


CONTAGIOUS  PLEURO^PNEUMONIA  IN  CATTLK 

Synonyms.  Lung  plague  ;  pleuro-pueumonia  zymotica  ; 
Peripnenmonie  contagieuse  :  Limgenseuche. 

^351.  Characterization.  Contagious  pleuro-pneu- 
nionia  of  cattle  is  a  specific  epizootic  disease  which  affects 
bovine  animals  and  from  which  other  species  are  exempt. 
When  the  disease  results  from  exposure  in  the  usual  manner, 
it  is  characterized  by  an  inflammation  of  the  lungs  and  pleurae, 
which  is  generally  extensive  and  which  has  a  tendency  to 
invade  portions  of  these  organs  not  primarily  affected  and  to 
cause  death  of  the  diseased  portion  of  the  lung. 

§  352  History.  The  first  account  of  the  appearance  of 
contagious  pleuropneumonia  dates  from  the  end  of  the  seven- 
teenth century.  It  is  stated  that  it  was  observed  in  Hesse  tor 
the  first  time  in  1693,  and  that  its  earliest  appearance  as  an 
epizootic  was  in  1713  and  1714,  when  it  prevailed  chiefly  in 
Switzerland  and  the  neighboring  countries  of  W  urtemberg, 
Baden  and  Alsace.  There  are  detailed  reports  of  its  occur- 
rence from  the  year  1743.  I"  ^773.  Haller  published  an  essay 
on  this  disease,  which  was  raging  severely  at  that  time.  He 
described  the  symptoms,  anatomical  characters  and  protective 
measures  laid  down  at  that  time  by  the  sanitary  police.  In 
17. S  the  disease  appeared  in  England  and  in  1765  m  France 
From  1790  it  spread  over  the  whole  of  Germany.  France  and 


442  CONTAGIOUS    PLEURO-PNEUMOXIA 

Ital}^  At  the  commencement  of  the  nineteenth  century  it 
visited  all  the  countries  of  Western  Europe. 

South  Africa  was  infected  b}'  a  bull  brought  from  Holland 
in  1854,  and  Australia  received  the  contagion  with  an  English 
cow  in  1858.  It  is  also  reported  as  existing  in  various  parts 
of  the  continent  of  Asia  ;  but  the  time  of  its  first  appearance 
and  the  extent  of  its  distribution  are  very  uncertain. 

Some  countries  which  have  only  been  infected  for  a  short 
time,  such  as  Norway,  Sweden  and  Denmark,  have  succeeded 
in  eradicating  the  disease  without  much  difficulty  by  slaugh- 
tering all  affected  and  exposed  animals.  Other  countries  long 
infected  and  in  which  the  contagion  was  thoroughly  estab- 
lished, like  Australia,  South  Africa,  Italy,  France,  Belgium 
and  parts  of  Germany,  have  labored  long,  in  some  cases  mak- 
ing no  progress  and  in  others  being  only  partially  successful. 
Holland  was  one  of  the  first  of  the  thoroughly  infected  coun- 
tries to  free  itself  from  the  contagion. 

The  disease  has  been  brought  to  the  United  States  several 
different  times.  Probably  its  first  introduction  was  in  a  dis- 
eased cow  sold  in  Brooklyn,  N.  Y.,  in  1843.  It  came  to  New 
Jersey  by  importing  affected  animals  in  1847.  Massachusetts 
was  infected  in  the  same  way  in  1859.  Massachusetts  eradi- 
cated pleuro-pneumonia  during  the  period  from  i860  to  1866. 
New  York  and  New  Jersey  made  an  attempt  to  eradicate  it  in 
1879  but  were  not  successful.  Late  in  1883  the  contagion  was 
carried  to  Ohio,  probabl)^  by  Jersey  cattle  purchased  in  the 
vicinity  of  Baltimore,  Md.,  to  which  place  it  had  extended 
previous  to  1S68.  From  the  herd  then  infected  it  was  spread 
by  the  sale  of  cattle  during  1884  to  a  limited  number  of  herds 
in  Illinois,  to  one  herd  in  Missouri  and  two  herds  in  Kentucky. 
By  cooperation  between  the  United  States  Department  of 
Agriculture  and  the  authorities  of  the  affected  states,  it  was 
found  possible  to  prevent  its  further  spread  and  to  completely 
eradicate  it  after  a  few  months. 

In  1886,  pleuro-pneumonia  was  discovered  in  some  of  the 
large  distillery  stables  of  Chicago  and  among  cows  on  neigh- 
boring lots.     This  led  to  renewed  efforts   to  secure    the    com- 


KKADICATIOX  443 

plete  extirpation  of  this  disease  from  the  country.  Congress, 
in  1887  enlar-ed  the  appropriation  available  for  this  purpose 
and  gave  more  extended  authority.  During  the  same  year  the 
disease  was  stamped  out  of  Chicago  and  has  not  since  appeared 
in  any  district  west  of  the  Allegheny  Mountains. 

The  work  of  eradication  was  at  the  same  time  commenced 
in  all  of  the  infected  States.  Before  the  end  of  the  year  1889 
Pennsylvania,  Delaware,  Maryland,  the  District  of  Columbia, 
and  Virginia  had  been  freed  from  the  disease.  More  difficul- 
ties however,  were  encountered  in  the  States  of  New  York 
and  New  Jersev  on  account  of  the  larger  territory  infected  and 
the  density  of  the  population.  The  long  struggle  was  crowned 
with  success,  however,  and  the  last  animal  in  which  the  dis- 
ease appeared  in  the  State  of  New  York  was  slaughtered  early 
in  1891  and  the  last  one  affected  in  New  Jersey  met  the  same 
fate  early  in  the  spring  of  1892. 

On  the  26th  dav  of  September.  1S92,  the  following  procla- 
mation was  issued,  declaring  the  United  States  to  be  free  from 
this  disease. 

PROCLAMATION -ERADICATION  OF  PLEURO-PNEUMONIA. 
U.  S.  Department  OF  AcRicri/ruRE, 

OFFICK  OF  THE  SKCRHTARV. 
To    ALL   WHOM    IT    MAY    CONCl'RX  : 

Notice  is  herebv  given  that  the  quarantines  heretofore  existing  in 
the  counties  of  Kings  and  Queens,  State  of  New  York,  and  the  counties 
of  Essex  and  Hudson,  State  of  New  Jersey,  for  the  suppression  ot  con- 
tagious pleuro-pneumonia  among  cattle,  are  this  day  removed 

The  removal  of  the  aforesaid  quarantines  completes  the  dissolving 
of  all  quarantines  established  by  this  Department  in  the  se^-eral  sections 
of  the  United  States  for  the  suppression  of  the  above-named  disease. 

No  case  of  this  disease  has  occurred  in   the  state  ot   Illinois  since 
December  29,  1887,  a  period  of  more  than  four  years  and  eight  months. 
No  case  has  occurred  in  the  state  of  Pennsylvania  since  September 
2Q    1888,  a  period  of  four  years  within  a  few  days. 

No  case  has  occurred  in  the  state  of  Maryland  since   September    iS, 

1889,  a  period  of  three  years. 


444  CONTAGIOUS    PLEURO-PNEUMONIA 

No  case  has  occurred  in  the  state  of  New  York  since  April  30,  1891, 
a  period  of  more  than  one  year  aiid  four  months. 

No  case  has  occurred  in  the  state  of  New  Jersey  since  March  25, 
1892,  a  period  of  six  months,  and  no  case  has  occurred  in  any  other 
portion  of  the  United  States  within  the  past  five  years. 

I  do  therefore  hereby  official!}-  declare  that  the  United  States  is  free 
from  the  disease  known  as  contagious  pleuro-pneumonia. 

J.   M.  RUSK,  Scctr/ary. 

Done  at  the  City  of  Washington,  D.  C,  this  26tli  day  of  September, 
A.D.,  1892. 

The  time  required  for  its  eradication  was  only  about  five 
years  and  the  total  expenditure  was  but  a  little  in  excess  of 
$1,500,000. 

§  353-  Etiology.  The  specific  cause  of  contagious 
pleuro-pneumonia  has  not  been  fully  demonstrated.  The 
infection  may  be  introduced  either  by  diseased  cattle,  or,  less 
commonly,  by  bearers  such  as  cattle  dealers,  attendants,  uten- 
sils, fodder,  dogs,  etc.  The  sheds  in  cattle  markets  are  very 
dangerous  centers  for  the  dissemination  of  the  disease.  All 
cattle  are  not  equally  susceptible.  It  is  generally  supposed 
that  about  one  animal  in  four  is  immune.  The  virus  is  spread 
principally  by  the  respired  air.  Infected  cattle  are  reported  to 
be  able  to  transmit  it  even  during  the  period  of  incubation, 
before  the  symptoms  are  apparent.  The  disease  is  particularly 
infectious  when  it  is  at  its  height  and  the  animal  remains 
capable  of  transmitting  the  disease  for  eight  or  ten  weeks  or 
even  longer  after  the  infection,  especially  when  necrotic  foci 
remain  in  the  lungs.  Walley  estimates  the  duration  of  infec- 
tiousness in  cases  of  encapsulated  necrotic  foci  to  be  as  long  as 
fifteen  months.  It  is  said,  but  the  evidence  is  not  given,  that 
the  virus  may  be  conveyed  by  the  respired  air  for  as  great  a 
distance  as  forty  yards  or  more.  In  exceptional  cases,  the 
contagium  is  transmitted  from  the  pregnant  cow  to    the    fetus. 

Pols  and  Noleu,  in  1886,  at  Amsterdam,  found  micrococci 
alway  present  in  the  exuded  matter  of  the  lungs.  These  mi- 
crococci were  about  0.9//  in  diameter  and  occurred  either  iso- 
lated or  in  chains  up  to   six    in    number.      In    the    unstained 


SYMPTOMS  445 


preparation,  the  cocci  were  surrounded  by  a  distinct  envelope 
which  could  be  stained  only  with  great  difficulty  and  which 
was  absent  from  cultivated  micrococci. 

Arloing  believed  that  he  had  found  the  existing  cause  of 
the  disease  hi  various  bacilli,  especially  in  one  which  he  calls 
Pneiivio-bacillns  liqiie/ade7is  bovis,  which  forms  short  nonmotile 
rods.  Arloing  believes  that  his  experiments  prove  that  the 
pneumo-baciUus  is  the  cause  of  pleuropneumonia. 

In  1898,  Nocard  and  Roux  succeeded  in  obtaining  a  very 
feeble  growth  of  an  exceedingly  minute  organism  in  bouillon 
containing  cow  or  rabbit  serum  in  proportion  of  one  part 
serum  to  25  parts  bouillon,  when  cultivated  in  collodion  sacs 
within  the  abdominal  cavity  of  rabbits.  The  rabbits  which 
received  the  inoculated  capsules  become  emaciated,  and  some 
of  them  died.  Those  inoculated  with  uninoculated  capsules 
remained  well.  Rabbits  inoculated  with  the  pleuropneumonia 
lungs  were  not  affected.  With  the  cultures  obtained  in  the 
collodian  sacs  the  disease  was  produced  in  cattle.  The  virus 
passed  through  a  Berkefeld  filter  and  Chamberland  F  cylinder 
but  it  was  held  back  by  a  Chamberland  filter  B. 

§  354.  Symptoms.  The  symptoms  are  such  as  would 
be  expected  with  inflammation  of  the  lungs  and  pleurae,  but 
they  varv  considerably  according  to  the  course  which  the 
disease  runs.  If  the  attack  is  an  acute  one,  as  is  frequently 
seen  in  hot  weather,  the  symptoms  appear  suddenly.  The 
breathing  becomes  rapid  and  difficult,  the  animal  grunts  or 
moans  with  each  expiration,  the  shoulders  stand  out  from  the 
chest,  the  head  is  extended  on  the  neck,  the  back  is  arched, 
the  temperature  ranges  from  104  to  107°  F.,  the  milk  secretion 
is  suspended,  there  is  loss  of  appetite,  rumination  is  stopped, 
the  animal  may  bloat  and  later  be  affected  with  a  severe 
diarrhea.  Such  cases  are  generally  fatal  in  from  seven  to 
twenty  da  vs. 

Very  often  the  attack  comes  on  slowly  and  the  symptoms 
are  more  obscure.  In  the  mildest  ca.ses  there  is  a  cough  for  a 
week  or  two  but  no  appreciable  loss  of  appetite  or  elevation  of 
temperature.     The  lungs  are  but  slightly  affected  and  recovery 


446  CONTAGIOUS   PLEURA-PNEUMONIA 

soon  follows.  Such  animals  may  disseminate  the  virus  for  a 
long  time  without  being  suspected  and  for  that  reason  are  the 
most  dangerous  of  all. 

A  more  severe  type  is  commonly  seen.  The  cough  is  fre- 
quently more  or  less  painful,  the  back  somewhat  arched  and 
the  milk  secretion  diminished.  These  symptoms  increase,  the 
appetite  is  affected,  the  animal  loses  flesh,  the  breathing 
becomes  more  rapid,  the  cough  more  painful,  pressure  of  the 
fingers  between  the  ribs  produces  evidence  of  tenderness,  the 
hair  loses  its  gloss  and  stands  erect,  the  skin  becomes  adher- 
ent, the  temperature  rises  to  103  to  105°  F.  Animals  thus 
affected  may  continue  to  grow  worse  and  die  in  from  three  to 
eight  weeks  or  they  may  after  a  time  begin  to  improve  and 
make  an  apparent  recovery.  The  inflammation  of  the  lung 
does  not,  as  a  rule,  subside  and  the  organ  does  not  return  to 
normal  condition  as  in  ordinary  pneumonia,  but  with  this  dis- 
ease the  life  of  the  affected  portion  of  the  lung  is  destroyed,  the 
tissue  dies  and  a  fibrous  wall  is  formed  around  it  to  shut  it 
away  from  the  living  parts.  The  tissue,  thus  encysted,  gradu- 
ally softens,  becomes  disintegrated  into  a  purulent-like  sub- 
stance.    The  recovery,  therefore,  is  only  partial. 

By  those  accustomed  to  examining  the  lungs  of  cattle, 
other  and  extremely  important  symptoms  may  be  detected 
during  the  course  of  the  disease.  By  auscultation  an  area  of  a 
certain  extent  may  be  found  where  the  natural  breathing 
sound  is  diminished  or  entirely  lost.  This  represents  the  dis- 
eased portion  of  the  lung.  In  other  cases  a  loud  blowing 
sound  may  be  heard,  quite  different  from  any  sound  produced 
when  the  lung  is  in  a  healthy  condition.  In  some  cases 
crepitation  is  heard  near  the  border  line  of  the  diseased  area 
and  friction  sounds  produced  by  the  roughened  pleura  may  be 
detected.  By  percussion  an  area  of  dullness  may  be  discov- 
ered corresponding  to  the  portion  where  the  respiratory  mur- 
mur has  disappeared.  This  loss  of  respiration  detected  by 
auscultation  and  the  dullness  brought  out  by  percussion  are 
the  most  important  evidences  of  an  area  of  inflamed  or  con- 
solidated lung. 


MORBID    ANATOMY  447 

Seriously  afifected  animals  remain  standing  if  they  have 
sufficient  strength,  but  those  which  lie  down  are  said  to  always 
lie  on  the  affected  side. 

The  proportion  of  animals  that  become  affected  after  being 
exposed  varies  according  to  the  virulence  of  the  outbreak,  the 
susceptibility  of  the  animals  and  the  length  of  time  during 
which  exposure  is  continued.  Sometimes  not  over  15,  20  or 
30  per  cent  of  the  animals  exposed  will  contract  the  disease, 
while  at  other  times  80  or  90  per  cent  may  be  infected.  The 
proportion  of  cases  in  which  the  disease  proves  fatal  also  varies 
greatly,  it  may  not  exceed  10  per  cent  and  it  may  reach  50 
per  cent.  In  general  it  may  be  said  that  about  40  per  cent  of 
the  exposed  animals  will  contract  the  disease  and  about  one- 
half  of  these  cases  will  prove  fatal. 

§  355.  Morbid  anatomy.  Anatomically,  contagious 
pleuro-pneumonia  is  characterized  by  a  progressive  interstitial 
pneumonia  with  secondary  hepatization  of  the  lungs  and  exu- 
dative pleuritis.  Usually  only  one  lung,  the  left  as  a  rule,  is 
affected.  The  anatomical  changes  vary  according  to  the  dura- 
tion of  the  disease. 

The  otherwise  healthy  lung  shows,  in  the  initial  stage, 
small,  circumscribed,  inflammatory  centers  from  the  size  of  a 
hazelnut  to  that  of  a  walnut.  The  interlobular  tissue  in  it 
is  hyperemic,  permeated  by  single  hemorrhages  and  infiltrated 
with  serum.  The  reddened  lobules  of  the  lungs  are  surrounded 
by  bright  margins,  which  are  i  to  2  ram.  broad  and  which 
are  filled  with  a  serous  or  lymphatic  fluid.  When  the  deposits 
are  superficial,  the  plurtc  become  opaque  and  covered  with 
slight  clots. 

At  the  height  of  the  disease  there  is  a  lobular  pneumonia 
with  pleuritis  which  is  usually  spread  over  the  greater  part  of 
one  lobe  of  the  lung.  The  lung  is  considerably  enlarged,  of 
firm  consistency,  very  heavy  (weighing  up  to  one  hundred 
pounds),  sinks  in  water  and  does  not  crackle  when  cut.  Its 
section  appears  marbled,  in  consequence  of  the  interstitial  con- 
nective tissue  having  become  thickened  into  broad  lines  which 


448  CONTAGIOUS    PLEURO-PNEUMONIA 

var}'  in  color  from  orange  to  dirtv  white  and  which  surround 
the  dark  colored  lobules  of  the  lung.  The  larger  lobules 
have  a  thickness  of  from  .2  to  5  cm.  ;  and  the  smaller  ones  of 
from  .25  to  .50  cm.  The  color  of  the  enclosed  lobules  of  the 
lungs  depends  on  the  duration  of  the  process  and  varies  from 
brown-red  to  dirt}'  yellow.  The  recently  infected  lobules  have 
a  blood-red,  reddish-brown  or  dark  brown  color  (stage  of  red 
hepatization).  The  color  of  the  older  ones  varies  from  orange 
to  yellow  (yellow  hepatization)  and  that  of  a  still  older  date  is 
gray  (gray  hepatization).  The  central  foci,  because  they  are 
the  oldest,  are  usually  in  a  stage  of  yellow  or  gray  hepatization. 
Some  of  the  enclosed  lobules  of  the  lungs  are  normal  or  only 
compressed,  while  others  are  merely  hyperemic.  If  we  closely 
examine  the  bright  interstitial  lines,  we  find  that  they  consist 
at  first  of  an  edematous  infiltration,  which  later  on  becomes 
plastofibrinous,  gelatinous,  indurated  and  finally  tends  to  the 
formation  of  adventitious  connective  tissue.  The  lymph-spaces 
in  the  lines  are  dilated  like  lacunae  and  filled  with  a  serous  or 
fibrinous  fluid.  In  robust  animals,  the  exudate  in  the  alveoli 
is  firm  ;  but  is  of  a  more  serous  character  in  animals  of  a  weak 
constitution.  In  the  former  case,  a  section  made  through  the 
lung  will  be  found  to  be  granular.  Besides  these  changes,  the 
other  13'mph  vessels  of  the  lungs  are  dilated,  their  walls  are  in- 
filtrated wfth  cells  and  their  lumen  is  in  a  state  of  thrombosis. 
The  blood  vessels  frequently  show  thrombi  and  small  hemor- 
rhagic infarcts.  The  contents  of  the  finer  bronchi  are  often 
infiltrated  with  numerous  white  corpuscles.  The  bronchial 
glands  and  frequently  the  mediastinal  glands  are  inflamed  and 
swollen. 

The  pleurae  are  covered  with  soft,  membranous,  fibrinous 
masses,  which  are  sometimes  lumpy  or  crumbled  and  which- 
can  easily  be  detached.  These  deposits  have  a  reticular  sur- 
face and  may  attain  a  thickness  of  2  cm.  If  we  remove  them, 
we  shall  find  the  pleural  vessels  highly  injected  with  ecchy- 
moses,  and  the  surface  of  the  pleurae  in  a  rough  and  uneven 
condition.  In  the  thoracic  cavity  we  generally  find,  in  vary- 
ing quantity,  an  inodorous  fluid  exudate,  which  may  be  clear 


MORBID    ANATOMY  449 


in 
rou 


or  opaque  and  which  contains  flakey  or  lumpy  masses.  Simi- 
lar fibrinous  masses  often  lie  on  the  outer  surface  of  the  peri- 
cardium. 

After  the  disease  has  existed  for   some  time,  the  affected 
parts  of  the  lungs  undergo  induration,  cicatrization,  caseation, 
calcification,  necrosis  or  suppuration.      At  first  the  inter.stitial 
infiltration   becomes  dense,   solid   and   dry   and  changes  into 
firm  connective  tissue  which  makes  a   crunching  noise   while 
it  is  being  cut  with  the  knife.      In  other   places  we  have  fatty 
degeneration,  caseation,  calcification  or  suppuration,  in  which 
the  enclosed  lobules  of  the  lungs,  in  consequence  of  the  exist- 
g  suppuration,  become  gangrenous,  and  form  sequestra  sur- 
ounded  by  sequestral  cavities  which  have  smooth  walls.     The 
dead  portions  of  the  lungs  may   remain  unchanged  in  these 
cavities  for  a  long  time.     Frequently  they  become  softened  to 
the  consistency  of  a  greasy,  yeast  like  paste.    Sometimes,  when 
they   are  comparatively   small,    they  become  absorbed,  and  a 
scar  is  formed.     The  hepatized  lobules  of  the  lungs  rarely  re- 
gain their  normal  condition  after  the  absorption  of  the  exudate. 
More  frequently  they  atrophy  or  collapse,  undergo  atelectasis, 
calcification   or  softening,  become   necrotic  or  suppurating  or 
form  cavities.     On   the   pleurae  we   find   thick   and  wart-hke 
hypertrophies  of   connective  tissue,   which  frequently    cause 
the  lungs  to  adhere  to  the  sides  of  the  chest. 

The  changes  in  the  lungs  and  pleurae  are  the  most  im- 
portant general  changes  in  cases  of  pleuro-pneumonia.  It  is 
stated  that  we  may  sometimes  meet  with  an  interstitial  fibrin- 
ous exudate  in  the  liver  with  atrophy  of  the  liver  cells  ;  sero- 
fibrinous effusions  into  the  articulations,  tendon  sheaths,  sub- 
cutis,  dewlap  and  brisket  ;  intestinal  catarrh  ;  areolation  ot 
Peyer's  patches  and  ulcers  on   the    gastro-intestinal    mucous 

membrane. 

The  views  of  pathologists  differ  as  to  the  nature  ot  the 
earliest  changes  in  contagious  pleuro-pneumonia  and  it  is  not 
within  the  scope  of  this  work  to  present  imperfectly  developed 
or  controverted  theories.  Without  entering  into  a  discussion  ot 
the  various  views,   it  is  clear  that  there   is  an    inflammatory 


450  CONTAGIOUS    PLEURO-PNEUMONIA 

condition  of  the  connective  tissue  between  the  lobules,  result- 
ing in  the  exudation  of  coagulable  lymph.  This  inflammation 
is  equally  marked  around  the  blood  vessels  and  air  tubes.  It 
leads  to  inflammatory  changes  in  the  inner  wall  of  the  veins 
and  these  cause  a  deposition  of  thrombi  or  plugs  in  the  vessels, 
which  prevent  the  return  of  the  blood.  The  blood  pumped 
into  the  lung  tissue  leaves  the  meshwork  of  capillaries  around 
the  air  vesicles,  enters  the  latter  and  produces  the  firm  hepa- 
tized  condition  so  characteristic  of  this  disease.  It  will  be 
easily  understood  how  the  different  shades  of  color  from  dark 
red  to  grayish  or  yellowish  red  are  produced  if  we  bear  in 
mind  that  the  veins  in  different  parts  of  the  lung  ti.ssue  are 
plugged  at  different  times  and  that  the  affected  regions  are  in 
different  stages  of  the  disease. 

One  of  the  most  conspicuous  features  in  a  microscopical 
section  from  a  lung  affected  with  acute  contagious  pleuro- 
pneumonia is  the  presence  of  intensely  stained  foci  and  lines^ 
These  lines,  to  which  Welch  seems  to  have  been  the  first  to 
call  attention,  are  visible  to  the  naked  eye  and  when  viewed 
with  a  hand  lens  suggest  by  their  peculiar  curves  the  contour 
lines  of  a  map.  They  are  situated  at  the  margin  of  and 
within  the  inflamed  connective  tissue  which  surrounds  the 
large  vessels  and  separates  the  lobules  from  one  another.  A 
closer  examination  ot  these  lines  indicates  that  they  coincide 
with  the  boundaries  of  the  lobules  and  of  the  individual  lymph 
spaces  of  the  interlobular  tissue.  Under  a  high  power  of  the 
microscope  they  are  resolved  into  dense  masses  of  leucocytes  in 
various  stages  of  degeneration.  These  dense  bands  are  pre- 
sumabl}''  attracted  to  the  connective  tissue  boundary  of  the 
lobules  and  to  the  walls  of  lymph  spaces  within  the  connective 
tissue  by  the  unknown  cause  of  the  'inflammation,  presumably 
the  cause  of  the  disease  itself.  The  space  between  the  lines  is 
filled  with  fibrin,  in  which  very  few  leucocytes  are  found. 

§  356.  Differential  diagnosis.  It  is  extremely  difficult 
to  form  an  exact  diagnosis  of  the  disease  during  its  develop- 
ment,   because   the  symptoms   which  are  present  are    few    in 


DIFPERKNTIAL    DIAGNOSIS  451 

number  and  b}-  no  means  characteristic.  The  slight  fever  and 
cough  are  the  only  symptoms  of  diagnostic  importance  in  the 
prodromal  stage.  In  the  second  or  acute  stage  a  positive 
diagnosis  i)it7-a  vitam  can  be  made  only  when  cases  of  pleuro- 
pneumonia have  previously  occurred  or  when  several  occur 
simultaneously.  As  a  rule,  a  correct  diagnosis  can  only  be 
made  by  a  post-mortem  examination.  The  following  diseases 
are  to  be  differentiated  from  it  :  — 

1.  Non-infedioits  iujlammation  of  the  lu7igs.  This  may 
be  distinguished  clinically,  as  a  rule,  by  its  more  acute  and 
more  typical  course  and  by  its  sporadic  and  sudden  appearance 
and,  anatomically,  by  the  fact  that  the  parts  which  have  under- 
gone hepatization  are  practically  all  of  the  same  age  and  that 
the  interstitial  lung  tissue  and  pleurae  are  but  slightly  involved. 
Nocard  states  that  in  exceptional  cases  pleuro-pneuraonia  may 
run  a  very  acute  course  and  show  hepatization  of  equal  ages. 

2.  Tuberculosis.  The  disease  cannot  be  positively  distin- 
guished clinically  from  pleuro-pneumonia.  Tuberculin  may  be 
used  as  a  diagnostic  agent,  although  it  is  not  at  all  certain 
that  animals  which  have  suffered  for  some  time  from  pleuro- 
pneumonia do  not  react  to  tuberculin.  After  all,  an  anatomi- 
cal examination  is  the  only  real  test.  Tuberculosis  and  con- 
tagious pleuro-pneumonia  have  occasionall}^  appeared  simul- 
taneously in  the  animal.  See  description  of  lesions  in  tuber- 
culosis. 

3.  Traumatic  pneumonia  or  pneumonia  due  to  foreign 
bodies  may  exhibit  the  same  symptoms  as  pleuro-pneumonia. 
Evidence,  during  life,  of  changes  in  the  heart  caused  by  trau- 
matic carditis  will  be  conclusive  in  making  the  differentiation. 

4.  Broncho  or  i7iie7'stitial pneumonia.  In  making  a  diag- 
nosis between  contagious  pleuro-pneumonia,  based  on  the  lung 
lesions  alone,  it  should  always  be  borne  in  mind  that  the  entire 
lung  should  be  subjected  to  examination.  Attention  should 
be  given  to  signs  indicating  injury  to  the  chest  wall,  to  the 
possible  presence  of  foreign  bodies  and  to  severe  inflammation 
of  the  air  passages  which  may    result  from   the   aspiration   of 


452  CONTAGIOUS  ,  PLEURO-PNEUMONIA 

irritant  or  corrosive  fluids.  Where  these  agents  may  be 
excluded  special  attention  should  be  paid  to  the  condition  of 
the  pleura  and  to  the  distribution  of  the  disease,  careful  notes 
being  made  of  the  lobes  involved.  Next  in  order  come  the 
peculiar  perivascular  and  interlobular  thickening  and  the 
thrombosis  of  the  veins.  Care  should  be  taken  not  to  con- 
found mere  clots  with  adhesive  thrombi.  In  acute  pleuro- 
pneumonia, after  death,  the  arteries  are  usually  distended 
with  clots.  The  different  features  of  the  hepatized  and 
edematous  portions  of  the  lung  ti.ssue  should  be  carefully 
noted.  Lastly,  the  peculiar  exudation  and  infiltration  in  the 
connective  and  fatty  tissue  of  the  dorsal  mediastinum  and  of 
the  embedded  glands  should  not  be  overlooked.  With  the 
microscope  the  peculiar  dense  cell  masses  of  the  diseased  con- 
nective tissue  should  be  looked  for  and  the  nature  of  necrotic 
tissue  determined  in  case  microscopical  appearances  are  no 
longer  reliable  owing  to  hardening  processes. 

Finally  it  should  be  borne  in  mind  that  the  lesions  of 
broncho-pneumonia  and  the  interlobular  changes  which  may 
follow  it  may  coexist  with  contagious  pleuro-pneumonia,  and 
that  both  kinds  of  lesions  may  be  encountered  in  the  same 
lungs.  Hence,  great  caution  must  be  exercised  in  expressing 
an  opinion  when  only  a. small  portion  of  the  lungs 'are  pre-  " 
sented  for  examination,  because  only  that  portion  which  is 
affected  with  broncho-pneumonia  may    have    been    submitted. 

§  357.  Preventive  inoculation  and  eradication.  '  In 
Europe  inoculation  has  been  practiced  for  a  long  time  as  the 
principal  means  for  combating  pleuro-pneumonia.  As  early 
as  the  beginning  of  the  last  century  it  was  proposed  in  Ger- 
many by  Hausmann  and  others.  Its  employment  was  greatly 
increased  by  the  investigations  which  were  made  in  1850  by 
Wilhelms  in  Holland  and  which  were  published  in  1852. 
Since  that  time  these  inoculations  have  been  practiced  in 
nearly  every  country.  The  literature  on  the  subject  is  very 
copious. 

The    advocates    of    inoculation,    among    whom    we    may 


PREVENTION  453 

mention  Haubner,  Bouley,  Schiitz  and  others,  start  from  the 
well  known  fact  that  one  attack  of  pleuro-pneumonia  success- 
fully passed  through  confers  immunity  for  the  remainder  of 
the  animal's  life.  By  inoculation,  a  local,  specific,  inflamma- 
tory  process  which  is  analogous  to  that  in  the  lungs,  is  pro- 
duced and  is  followed  by  subsequent  immunity  of  the  whole 
body.  Haubner  calculates  that  the  mortality  from  the  inocu- 
lation is  from  I  to  2  per  cent  and  that  the  tips  of  the  tails  are 
lost  in  from  5  to  lo  per  cent  of  the  cases.  In  Holland,  among 
59,180  cattle  inoculated  in  1878  and  1879,  the  mortality 
amounted  to  only  0.66  per  cent. 

The  opponents  of  inoculation,  among  whom  we  may  men- 
tion Rolof,  Ziindel,  Kitt,  M'Fadyean  and  others,  assert  that 
up  to  the  present  no  positive  case  of  immunity  has  been  proved 
to  have  been  obtained  from  inoculation.  They  also  point  to 
the  fact  that  even  the  advocates  for  inoculation  are  unable  to 
give  the  exact  duration  of  the  immunity  and  consequently 
make  several  inoculations.  Dujardin-Beaumetz  finds  that  the 
inoculation  in  the  tail  with  a  bouillon  culture  of  the  organism 
gives  a  local  swelling.  It  confers  immunity  quite  as  well  as 
the  injection  of  the  serous  fluid.  Already  he  reports  its  use 
in  675  cattle,  of  which  14  died  as  a  result  of  the  inoculation. 
The  best  procedure  seems  to  be  the  stamping  out  of  the  dis- 
ease by  means  of  thorough  disinfection  or  destruction  by  fire 
of  all  infected  sheds  and  barns.  The  success  of  this  method 
is  illustrated  by  the  eradication  of  the  disease  from  the  I  nited 
States. 

RKFERKNCES 

I.  DUJARDIN-BEAUMETZ.  Le  microbe  cle  la  peripneumonie  et  la 
culture.      Thesis.     Paris,  1900. 

2  NOCARD  ET  Roux.  Le  microbe  de  la  peripneumonie.  Recueil 
de  Med  VHerinaire,  March  24,  1898,  p.  212.  i  Trans,  m  the  Veterinary 
Journal,  London,  Vol.  XLVII  (1898),  p.  147-  Ann.  dc  V Inst.  Pasteur, 
Vol.  XII  (1898),  p.  240.) 

3.  Salmon.  Annual  Reports  0/ th^  Bureau  0/ Animal  Industry, 
I 884-1892. 

4.  SMITH.     Annual  Report  of  the  Bureau  of  Animal  Industry, 

1895-6,  p.  143- 


454  FOOT    AND    MOUTH    DISEASE 

5.  Walley.     The  four  bovine  scourges.     1879. 

6.  WllvHELMS.       Memoire    sur    la   peripneumonie  epizootique  du 
betail,  1852. 


FOOT  AND  MOUTH  DISEASE 

Synonyms.  Eczema  epizootica  ;  epizootic  aphtha  ;  vesi- 
cular aphtha  ;  vesicular  epizootic  ;  aphthous  fever  ;  murrain  ; 
cocotte ;  MaiU-iind  Klaue7iscnche. 

§  358.  Characterization.  Foot  and  mouth  disease  is 
a  highly  infectious  disease  of  animals.  It  is  determined  by 
the  eruption  of  vesicles  in  the  mouth,  around  the  coronet  of 
the  foot,  on  the  udder  and  between  the  toes.  It  is  said  to  be 
more  common  among  cattle,  but  swine  are  quite  susceptible  ; 
sheep,  goats,  horses,  dogs,  cats  and  fowls  are  said  sometimes 
to  be  attacked.  The  human  species  is  also  susceptible.  Peo- 
ple may  be  infected  by  drinking  the  unboiled  milk  of  animals 
suffering  from  the  disease.     The  mortality  is  not  high. 

§  359-  History.  Foot  and  mouth  disease  was  quite 
accurately  described  in  the  eighteenth  century.  \'ery  destruc- 
tive outbreaks  are  reported  in  1809  and  in  the  early  part  of  the 
nineteenth  century  it  was  the  source  of  much  loss  in  southern 
Europe.  In  1883,  Great  Britain  lost  heavily  from  its  ravages. 
In  1892,  Prussia  is  reported  to  have  had  8,000,000  cattle 
affected.  It  was  during  the  years  1890  and  1893  that  the  last 
severe  epizootic  appeared  in  Germany. 

§360.  Geographical  distribution.  This  disease  seems 
to  be  very  largely  restricted  to  Europe,  although  it  has  been 
introduced  into  almost  every  cattle  raising  country.  In  1870, 
it  was  brought  to  the  United  States  from  Canada.  At  that 
time  it  spread  into  New  York  and  New  England.  It  appears 
that  this  disease  was  mild  and  its  spread  was  quickly  and 
easily  checked.  This  according  to  Law  was  accomplished  so 
easily  because  the  cattle  were  in  winter  quarters.  In  1880,  a 
few  infected  animals  were  brought  to  the  United  States,  but 
the  disease  did  not  extend  bevond  the  animals  introduced.      In 


ETIOLOGY  455 

1884,   there  was  a  small    epizootic    at     Portland    caused    by 
imported  cattle. 

The  most  serious  outbreak  in  the  United  States  was  in 
1Q02.  The  first  herds  affected  were  at  Chelsea,  Mass.,  in  the 
vicinity  of  the  docks,  to  which  place  the  infection  was  probably 
carried  from  shipping.  It  is  not  known  exactly  how  the  infec- 
tion was  introduced,  but  it  is  highly  probable  that  it  came 
through  some  one  of  the  many  possible  channels  other  than 
infected  imported  cattle.  In  this  outbreak,  the  disease  ap- 
peared in  Massachusetts,  New  Hampshire,  Vermont  and 
Rhode  Island.  A  total  of  4.712  cattle  were  affected.  The 
comparative  freedom  of  the  United  States  from  this  disease  is 
attributed  to  the  enforcement  of  rigid  quarantine  measures. 

§  361.     Etiology.     The  specific  cause  of  foot  and  mouth 
disease  has  not  been  clearly  demonstrated.     It  has  been  shown, 
however,  that  it  is   caused   by   a   specific   infection    and    that 
every  outbreak  starts  from  some  previous  case  or  cases.     The 
virus  is  contained  in  the    eruptions    and    given    off    from    the 
mouth  and  feet,   causing  its  wide  distribution.     Loeflfler  and 
Frosch  have  shown  that  the    cause— presumably  a    germ    of 
some  form-would  pass   through    a   Berkefeld   filter.       Uater 
Loeffler  showed  that  it  did  not  pass  through  the  finer  kitasato 
filter      Animals  may  be  infected  directly  by    coming   in   con- 
tact with  the  disease,  or  indirectly  by    being   exposed    to    the 
virus  in  stables,    cars   or   other   places   recently  occupied   by 
infected  animals.     It  is  stated  that  the  virus  is  destroyed  in  a 
short  time  by  drying,  but  some  writers  maintain    that    it    wiU 
persist  for  several  months.     Penberthy  states  that  under  ordi- 
nary circumstances  the  virus  does  not  retain    its   effectiveness 
lono-      Animals  that  have  passed    through    the   disease    may 
carry  the  virus  for  several  months.     The  infected  matter  may 
be  carried  on  the  clothing  or  hands  of  human  beings  and  thus 
be  transmitted  to  animals  or  men.      Milk  is  often  the  carrier  of 

the  virus. 

The  period  o/mcHbatwn\ss\mn,iron\  2^  io    -2    hours   in 

inoculated  cases.     It  may  be  longer  than  this. 


456  FOOT    AND    MOUTH    DISEASE 

^  362.  Symptoms.  The  symptoms  of  foot  and  mouth 
disease  vary  greatly  in  different  epizootics,  sometimes  they  are 
quite  mild  and  at  others  very  severe.  The  first  evidence  of 
the  disease  is  a  rise  of  temperature  which  in  cattle  rarely 
exceeds  104°  F.  The  mucous  membrane  of  the  mouth  becomes 
reddened,  the  appetite  is  diminished,  and  rumination  ceases. 
The  mouth  is  usually  kept  closed  and  the  quantity  of  saliva  is 
increased.  A  smacking  sound  is  not  infrequently  made  by  the 
animal.  These  symptoms  are  chiefly  due  to  the  pain  accom- 
panying the  disease  in  the  mouth.  After  two  or  three  days 
the  eruption  appears.  This  consists  of  small  yellowish-white 
vesicles  or  blisters,  varying  in  size  from  a  hemp  seed  to  a  pea, 
on  the  gums  and  inner  surface  of  the  lips,  the  inside  of  the 
cheeks,  the  border  and  the  under  surface  of  the  tongue.  Thej' 
may  become  half  an  inch  or  more  in  diameter.  In  some  cases 
the  back  of  the  tongue  may  be  the  seat  of  large  blisters. 

These  vesicles  burst  soon  after  their  appearance,  some- 
times on  the  first  day.  More  rarely  they  may  persist  for  two 
or  three  days.  After  they  have  ruptured  the  grayish-white 
membrane  forming  the  blister  may  remain  for  a  day  or  more 
or  disappear  speedily  and  leave  deeply  reddened  areas  or  ero- 
sions which  are  very  painful.  These  exposed  areas  may  soon 
become  covered  again  with  the  normal  epithelium  or  they  may 
be  converted  into  ulcers.  In  this  stage  the  saliva  forms  in 
large  quantities  and  hangs  in  strings  from  the  mouth.  In 
eight  to  fourteen  days  the  disease  may  have  entireh'  disap- 
peared. 

In  addition  to  the  changes  in  the  mouth,  one  or  more  feet 
may  become  diseased.  The  skin  around  the  coronet  and  in 
the  cleft  between  the  toes  becomes  hot  and  tender  and  may 
swell.  Blisters  appear  as  in  the  mouth,  but  they  are  speedily 
ruptured  and  the  inflamed,  exposed  areas  are  covered  with  a 
viscid  exudate. 

The  udder,  more  particularly  the  teats,  may  be  the  seat  of 
lesions.  Some  authorities  regard  the  udder  di.sease  merely  as 
the  result  of  infection  during  milking.  The  vesicles  are 
broken  by  the  hands  of  the  milker  and  the  teats  become  cover- 


MORBID    ANATOMY  457 

€d  with  reddened  areas  deprived  of  the  superficial  layer  of  the 
skin  and  are  very  tender.  The  healing,  however,  goes  on 
quite  rapidly.  The  milk  is  said  to  be  somewhat  changed  in 
appearance  and  unfit  for  making  butter  or  cheese.  These  are 
the  main  symptoms  accompanying  the  uncomplicated  cases  of 
foot  and  mouth  disease.  In  all  such  cases  recovery  is  usually 
rapid  and  complete.  In  certain  other  cases,  however,  compli- 
cations arise  which  are  not  only  injurious  but  may  be  fatal. 
Thus  the  mouth  lesions  may  be  accompanied  by  nasal  catarrh 
or  pneumonia.  The  feet  may  become  very  much  swollen  and 
the  inflammation  and  suppuration  extend  to  the  tendons  and 
bones,  resulting  in  the  loss  of  the  hoof.  Such  cases  are  usual- 
ly fatal.  Asa  result  of  the  general  affection  young  calves  may 
succumb  to  a  secondary  inflammation  of  the  stomach  and 
bowels  and  older  animals  ma\-  abort  or  suffer  from  inflamma- 
tion of  the  udder. 

The  duration  of  the  disease  \\\  uncomplicated  cases  varies 
from  10  to  20  days.  When  complications  occur  either  with 
the  regular  course  or  as  sequelae  the  duration  becomes  indefi- 
nite. The  mortality  varies  with  the  severity  of  the  attacks, 
the  age  and  condition  of  the  animals  and  the  treatment. 
Ordinarily  the  mortality  is  not  high,  excepting  in  very  young 
animals. 

v^  363.  Morbid  anatomy.  The  tissue  changes  found  at 
post-mortem  vary  to  a  marked  degree.  There  are  in  certain 
cases  hyperemia  and  edema,  catarrh  of  the  nares  and  mucosa 
of  the  lungs  and  dilatation  of  the  heart.  There  may  be  fatty 
degeneration  and  hemorrhagic  infarcts  in  the  heart  muscle. 
In  other  cases  there  is  severe  gastro- enteritis  with  intestinal 
hemorrhage.  In  the  stomachs  of  cattle  oval  reddish  areas 
which  ultimately  form  ulcers  appear.  These  often  become 
confluent.  The  involved  portion  of  the  mucous  membrane 
becomes  thickened.  The  areas  of  necrotic  tissue  in  which  the 
ulcers  appear  become  surrounded  by  a  reddish  line  of  demar- 
cation which,  in  the  healing  process,  forms  a  cicatrix.  The 
lesions  on  the  mucous   membrane   rarely  extend    deeper    than 


45^  FOOT    AND    MOUTH    DISEASE 

the  mucosa.  Ulcers  of  a  nature  similar  to  those  found  in  the 
stomach  occur  in  the  intestines.  On  the  feet  inflammations 
may  follow  the  simple  vesicles  about  the  coronet.  These  may 
extend  deep  into  the  tissues,  pass  under  the  hoof  and  cause  it 
to  slough  off,  extend  into  the  bone  producing  necrosis  or 
permanent  arthritis.  It  is  stated  by  some  authorities  that  in 
the  mild  non- fatal  cases  the  obvious  lesions  are  so  slight  that 
frequently  they  escape  notice.  In  sheep  and  swine  the  lesions 
are  more  frequently  restricted  to  the  feet. 

The  period  of  dicratkni  oi  \h&  d\SQ2ise  \3ix\es  from  9  to  14 
days.  The  immunity  resulting  from  a  natural  course  of  the 
disease  is  placed  by  Penberthy  as  being  brief,  probably  not  to 
exceed  six  months. 

S  364.  Differential  diagnosis.  Foot  and  mouth  dis- 
ease must  be  differentiated  from  (i)  various  forms  of  stoma- 
titis caused  by  different  fungi  and  often  referred  to  as  sporadic 
aphthae,  (2)  from  stomatitis  due  to  drugs  and  injuries,  (3) 
from  actinomycosis  of  the  tongue  and  (4)  from  variola.  It 
must  also  be  differentiated  from  simple  cellulitis,  often  of 
streptococcic  origin,  in  the  subcutaneous  tissue  about  the 
coronet  and  from  the  sloughing  of  the  hoof  resulting  from  the 
extension  of  the  inflammatory  process,  and  from  eczemas  due 
to  dietary  causes.  The  means  of  differentiating  these  must  be 
found  largely  in  the  history  of  the  cases  and  in  the  study  of 
the  nature  of  the  lesions  themselves. 

§  365.  Prevention,  Preventive  inoculations  do  not 
seem  to  have  given  satisfactory  results.  The  isolating  of  the 
diseased  animals  and  the  placing  of  the  well  ones  in  non-in- 
fected fields  and  stables  tend  very  largely  to  the  checking  of 
the  spread  of  the  disease.  The  milk  of  the  diseased  animal 
should  be  sterilized  before  it  is  used. 

In  England  the  slaughter  of  infected  animals  has  fre- 
quently been  resorted  to  in  recent  years  to  stamp  out  the  dis- 
ease. In  the  recent  outbreak  in  the  United  States,  the  prompt 
destruction  of  all  infected  and  exposed  animals  proved  to  be 
very  satisfactory.     The  failure  in  the  past   to  control   the    dis- 


ClIAKACTKRIZATION  459 

ease  in  Europe  bv  quarantine  and  disinfection  necessitated  the 
radical  measure  of  slaughter  of  infected  and  exposed  animals 
in  order  to  eliminate  the  disease  from  our  country. 

Loeffier  has  recently  produced  artificial  immunity  against 
this  infection  by  a  method  which  promises  to  be  successful  for 
practical  immunization. 

REFKRRNCKS. 

1  Coi'K  Foot  and  mouth  disease.  Re.poU,  7th  International 
Congress  of  Vet.  Surgeons.     Iladcn  Baden,  Vol.  I  (1899),  P-  '84. 

2  LOEFFLER  UND  Frosch.  Berichte  der  Komniission  x.ur  Erfor- 
schung  der  Maul  uud  Klaueuseuche  bei  dem  Institut  fUr  Infektious 
Krankheiten  in  Berlin.     Cent,   f  BaM.     Bd.  XXIII  (.898),  S.  37i- 

3.     LOEFFLER.     Ibid,     Bd.  XXIV  (1898),  S.  569- 

4  LOEFFLER.  Ein  neuer  Verfahren  der  Schut/.impfung  gegen 
Maul  und  Klauenseushe.     Munch.  Med.    II 'oc/iensc/ir.,  1906.     S.  1036. 

5.  PENBERTHV.  Foot  and  mouth  disease.  Jour.  Comf.  Path, 
and  T/iera.,  Vol.  XVI  (  1901),  p.  16. 

b  P..-TERS  Foot  and  mouth  disease.  Second  Semi-annual 
Report  of  the  Chief  of  the  Cattle  Bureau.  Mass.  State   Board  of  Agric. 

1903.    P-    321-  ,      ,,      C      /I    A/       ^Z- 

7  SALMON-  Foot  and  mouth  disease.  Year  hook  U.  S.  Dcpt.  oj 
Agric.  "1902.  p.  643.  Ibni.  Annual  Report  Bureau  of  Animal 
Industry,  1902,  p.  391. 

8.     W.\LLEY.     The  four  bovine  scourges.     1879-     P-  ^i- 


RABIES 

Synonyms.  Hydrophobia  ;  canine  madness  ;  lyssa;  Rage  ; 
Tolhvnt ;    Wutkrankheit. 

§  366.  Characterization.  Rabies  is  an  acute  infectious 
disease  transmitted  from  animal  to  animal  or  from  animal  to 
man  bv  the  bite  of  the  rabid  individual  or  by  direct  inocula- 
tion It  is  not  known  to  be  contracted  or  tran.smitted  in  any 
other  manner.  It  is  characterized  by  a  long  and  variable 
period  of  incubation,  followed  by  symptoms  referable  to  the 
nervous  svstem,  lasting  from  one  to  ten    days    and    ending    in 


460  RABIES 

paralysis  and    death,    without   recognizable   gross    anatomical 
changes. 

The  dog  is  the  animal  most  commonly  affected,  although 
all  of  the  canine  and  feline  races  seem  to  suffer  from  rabies 
more  than  other  species.  All  warm  blooded  animals  appear  to 
be  susceptible.  It  is  a  serious  disease  in  man,  cattle,  sheep, 
horses  and  swine.  An  explanation  for  its  greater  frequency 
among  dogs  is  found  in  their  tendency  to  bite.  A  very  large 
percentage,  in  fact  nearly  all,  of  the  cases  in  man  and  in  the 
domesticated  animals  are  caused  by  inoculation  from  the  bites 
of  rabid  dogs. 

§  367.  History,  Rabies  was  described  by  Aristotle  in 
the  fourth  century  B.  C.  Rewrote.  "Dogs  suffer  from  mad- 
ness that  puts  them  in  a  state  of  fury,  and  all  the  animals  that 
they  bite,  when  in  this  condition,  become  also  attacked  by 
rabies."  Cornelius  Celsius,  who  lived  in  the  first  part  of  the 
Christian  era,  seems  to  have  been  the  first  to  refer  to  human 
rabies  and  to  employ  the  term  "hydrophobia." 

The  transmission  of  the  disease  by  wolves  to  man  was 
recorded  in  159 1.  In  1803,  and  for  a  number  of  years  follow- 
ing, it  was  epizootic  among  foxes  in  Southern  Germany  and 
Switzerland. 

During  the  latter  part  of  the  eighteenth  and  the  beginning 
of  the  nineteenth  century  the  disease  extended  over  Europe 
and  about  this  time  it  appeared  in  America.  The  first  out- 
break in  this  country  was  reported  from  Boston  in  176S.  In 
1770  and  1 77 1  it  was  observed  in  dogs  and  foxes  in  the  vicinity 
of  Boston  ;  in  the  year  1779  it  appeared  in  Philadelphia  and 
in  the  state  of  Maryland  ;  in  1785  it  was  prevalent  throughout 
the  Northern  States  and  soon  after  it  spread  to  the  Southern 
States.  During  the  last  century  it  has  caused  heavy  losses 
among  farm  animals  throughout  E^urope  and  America. 

It  has  called  forth  careful  study  from  many  of  the  ablest 
men  in  the  medical  professions.  Among  them  may  be  men- 
tioned John  Hunter  in  England,  Viborg  in  Copenhagen,  Wal- 
dinger  in  Vienna,  Hertwig  in  Germany  and  Pasteur  in  France. 


GEOC.RU'HICAI.    DISTRIHUTION  46 1 

Without  detracting  in  the  least  from  the  great  work  of  other 
investigators,  we  may  say  that  to  Pasteur  and  his  co-laborers, 
Nocard'and  Roux,  we  owe  much  of  the  knowledge  ot  the 
nature  of  rabies  which  we  possess  at  the  present  time. 

ii  368.  Geographical  distribution.  Rabies  is  known 
to  exist  in  almost  every  country  on  the  globe.  Australia  is 
the  largest  area  which  is  said  to  be  absolutely  free  from  it. 
This  exemption  is  the  gratifying  result  of  a  rigid  quarantine 
enforced  against  dogs  imported  on  that  island.  Rabies  is  very 
common  in  France,  Belgium  and  Russia.  In  the  latter 
country  it  is  perhaps  more  often  seen  in  wolves  than  in  any 
other  part  of  the  world.  In  Holland,  Denmark  and  Sweden  it 
is  very  rare.  In  England,  it  has  from  time  to  time  been  wide- 
spread, but  at  present  it  is  practically  eradicated.  Salmon 
has  found  that  rabies  exists  in  nearly  every  part  of  the  United 

States. 

Inquiries  which  the  writer  has  made  during  the  last  tew 
years,  by  verifying  current  newspaper  reports  of  rabies,  show 
that  the  larger  number  of  cases  come  from  certain  districts  in 
which  the  disease  seems  to  have  become  established.  Newly 
infected  districts  are  constantly  springing  up,  due  presumably 
to  the  introduction  in  some  manner  of  an  infected  dog. 

The  prevalence  of  the  disease  cannot  be  accurately  deter- 
mined, as  there  are  no  reliable  statistics  concerning  it. 
Ravenel  has  reported  that  the  State  Live  Stock  Sanitary  Board 
of  Pennsvlvania  has  investigated  82  cases  of  rabies  since  1897. 
Of  these  there  were  58  dogs,  4  horses,  17  cows,  i  cat  and  2 
human  beings.  During  i90o-'o4  the  New  York  State  Veteri- 
nary College  investigated  64  cases  of  rabies,  of  which  47 
were  in  dogs,  11  in  cattle,  2  in  horses,  i  in  sheep,  i  in  swine, 
and  2  in  men.  In  1907  a  much  larger  number  of  cases  were 
presented  for  diagnosis.  Salmon  states  that  in  the  District  of 
Columbia  from  1893  to  August  1900  rabies  has  been  positively 
diagnosed  in  animals  in  91  cases.  These  consisted  ot  80  dogs, 
5  cows,  2  horses,  2  foxes  and  2  cats.  In  addition  to  these  the 
records  of  the  health  department  of  the  District  of  Columbia 
show  that  since  1874  there  have  been  seven  deaths  from  rabies 


462  RABIES 

in  the  human  species.  These  illustrations  from  the  experi- 
ences of  a  few  laboratories  could  be  duplicated  from  the  records 
of  many  others. 

In  Europe  the  disease  seems  to  be  more  prevalent.  In 
1898  the  official  reports  show  1,202  cases  of  rabies  in  animals 
(most]}'  dogs)  in  German}-.  In  1899,  2,374  rabid  animals 
were  reported  from  France  and  444  cases  from  Belgium. 


Fig.  1 10.  A  draiL'ing  from  a  section  of  a  rabid  brain,  s/ioiuttig  large 
nerve  cells  containing  Negri  bodies,  {a)  Nerve  cell,  {b)  nucleus  of 
nerve  cell,  [c)  Negri  bodies.     Much  enlarged. 

§  369.  Etiology.  Although  rabies  has  long  been  recog- 
nized as  a  specific  disease,  its  primary  etiological  factor  has  but 
recently  been  discovered  by  Negri  in  the  brain  and  spinal  cord 
of  the  affected  animal.  In  certain  instances  the  presence  of 
the  virus  has  been  reported  in  the  salivary  glands,  pancreas 
and  milk.     It  has  not  been  found  in  the  blood. 

In  1903,  Negri,  of  the  University  of  Pavia,  described 
small  bodies  or  cell  inclusions,  since  called  Negri  bodies,  which 
he  found  in  the  Purkingie  cells  of  the  cerebellum    and    in    the 


ETIOLOGY  4^13 

large  ganglion  cells  of  the  Amnions  horn.  Negri  believed 
these  bodies  to  be  the  etiological  factor  of  the  disease  and  clas- 
sified them  among  the  protozoa. 

He  believes  the  bodies  are  specific  microorganisms  which 
are  characteristic  of  the  disease,  found  only  in  animals  affected 
with  rabies.  They  appear  early  in  the  course  of  the  disease. 
They  occur  in  larger  numbers  and  are  of  greater  size  as  the 
disease  progresses.  They  are  most  numerous  and  largest  at 
the  time  of  death.  Smears  or  sections  are  stained  in  saturated 
alcoholic  solution  of  eosin  for  from  10  to  30  minutes  after  which 
they  are  counter-stained  in  alkaline  methylene  blue.  No 
special  technique  is  necessary  to  demonstrate  these  bodies. 
Their  constant  appearance  in  cases  of  rabies  forms  a  basis  for  a 
positive  opinion  and  diagnosis  and  they  are  affected  very  little 
by  beginning  decomposition  of  the  surrounding  nervous  tissue. 

Williams  and  Lowden  state  concerning  the  channels  of 
infection  that  "in  whatever  way  the  virus  enters  the  body,  so 
far  as  we  know,  there  is  no  development  of  the  organism,  or 
none,  to  any  appreciable  extent,  until  it  reaches  the  central 
nervous  system,  and  not  until  after  a  certain  amount  of  deve- 
lopment there  does  it  infect  the  peripheral  organs.  Before  the 
disease  was  well  studied  it  was  thought  that  the  salivary  glands 
were  the  chief  site  of  the  infection.  But  it  has  been  shown 
that  these  glands  are  not  always  infective,  and  when  they  are, 
not  until  comparatively  late  in  the  disease  and  that  when  the 
virus  is  inoculated  into  tUem,  the  animal  .seldom  comes  down 
with  the  disease  and  probably  never  if  the  centripetal  nerves 
are  cut  (Bertarelli).  This  means  that  the  parasite  does  not 
grow  in  the  salivary  glands,  that  it  is  only  carried  there  inci- 
dentally by  its  spread  from  the  central  nervous  system  along 
the  nerve  branches.  That  the  organisms  escape  into  the  blood 
and  are  carried  in  this  way  in  small  numbers  is  shown  by  the 
fact  that  the  blood  in  large  quantities  has  been  found  infective 
(Marie).  Principally  by  the  nerve  channels,  secondarily  by 
the  blood  and  lymph  channels,  the  organisms  are  carried  in 
small  numbers  to  all  parts  of  the  body.  With  other  investiga- 
tors, we  have  found  the  suprarenal  cepsules  infective."     Their 


464  RABIES 

conclusion  relative  to  the  nature  and   diagnostic  value  of  the 
Negri  bodies  are  as  follows  : 

1.  The  smear  method  of  examining  the  Negri  bodies  is 
superior  to  any  other  method  so  far  published  for  the  follow- 
ing reasons  :  (a)  It  is  simpler,  shorter  and  less  expensive  ;  (b) 
The  Negri  bodies  appear  much  more  distinct  and  characteristic. 
For  this  reason  and  the  preceding  one,  its  value  in  diagnostic 
work  is  great  ;  (c)  The  minute  structure  of  the  Negri  bodies 
can  be  demonstrated  more  clearly  ;  (d)  Characteristic  staining 
reactions  are  brought  out. 

2.  The  Negri  bodies  are  shown  by  the  smears  as  well  as 
by  the  section  are  specific  to  hj'drophobia. 

3.  Numerous  "bodies"  are  found  in  fixed  virus. 

4.  "Bodies"  are  found  before  the  beginning  of  visible 
symptoms — i.  e.,  on  the  fourth  day  in  fixed  virus,  on  the 
seventh  day  in  street  virus,  and  evidence  is  given  that  the}' 
may  be  found  early  enough  to  account  for  the  appearance  of 
infectivity  in  the  host  tissues. 

5.  Forms  similar  in  structure  and  staining  qualities  to 
the  others,  but  just  within  the  limits  of  visible  structure  at 
(1,500  diam.  magnification)  have  be  seen.  Such  tiny  forms, 
considering  the  evidence  they  give  of  plasticity,  might  be  able 
to  pass  the  coarser  Berkefeld  filters. 

6.  The  Negri  bodies  are  organisms  belonging  to  the  class 
Protozoa.  The  reasons  for  this  conclusion  are  :  (a)  They 
have  a  definite,  characteristic  morphology  ;  (b)  This  morpho- 
logy is  constantly  cyclic,  i.  e.,  certain  forms  always  predomi- 
nate in  certain  stages  of  the  disease,  and  a  definite  series  of 
forms  indicating  growth  and  multiplication  can  be  demon- 
strated ;  (c)  The  structure  and  staining  qualities  as  shown 
especially  by  the  smear  method  of  examination  resembles  that 
of  certain  known  Protozoa,  notably  of  those  belonging  to  the 
sub-order  Microsporidia. 

7.  The  proof  that  the  "Negri  bodies"  are  living  organ- 
isms is  sufficient  proof  that  they  are  the  cause  of  hydrophobia  ; 
a  single  variety  of  living  organisms  found  in    such  large  num- 


ETIOLOGY  465 

bers  in  every  case  of  a  disease,  and  only  in  that  disease, 
appearing  at  the  time  the  host  tissue  becomes  infective  in 
regions  that  are  infective,  and  increasing  in  these  infective, 
areas  with  the  course  of  the  disease,  can  be  no  other,  accord- 
ing to  our  present  views,  than  the  cause  of  that  disease. 

The  Negri  bodies  or  cell  inclusions  vary  in  shape.  The 
most  common  forms  are  round  or  oval.  The  round  bodies  are 
from  .5  to  231.1  in  diameter,  while  the  oblong  ones  vary  from 
.5  to  15//  to  5  to  2J/1.  The  round  or  oval  forms  are  by  far  the 
most  common.  Irregular  forms  are  occasionally  seen.  In 
preparations  stained  with  eosin  and  methylene  blue  they  ap- 
pear as  bright  red  bodies  containing  one  or  two  nuclear-like 
structures  which  are  surrounded  by  a  number  of  other  small 
circular,  regular  bodies.  They  are  said  to  preserve  their  form 
even  when  the  brain  tissue  has  undergone  marked  degenera- 
tive changes,  after  prolonged  immersion  in  glycerin  and  after 
several  days'  drying.  A  number  of  workers  report  finding 
them  quite  uniformly.  Schuder  does  not  consider  them  as 
the  cause,  largely  because  his  virus  passed  through  a  filter  that 
retained  the  cholera  spirillum. 

Remlinger  and  Riffat-Bey  found  that  the  virus  would 
pass  through  a  Berkefeld  filter  "V,"  but  its  passage  was  not 
constant,  as  rabbits  inoculated  with  the  filtrate  did  not  all  die 
of  rabies.  The  filter  which  he  used  held  back  the  organism 
of  chicken  cholera,  which  was  used  as  a  check  on  the  filter. 
Remlinger  more  recently  stated  that  the  virus  will  pass  through 
the  more  porous  Berkefeld  filter  only.  The  firmer  Berkefeld 
and  Chamberland  filters  keep  the  virus  back. 

Babes  states  that  the  Negri  bodies  are  not  always  present. 
He  seems  to  consider  them  as  a  result  of  the  local  reaction  of 
the  cells  to  the  cause  of  the  disease. 

i^  370.  Method  of  invasion.  When  introduced  into  an 
animal  either  experimentally  or  by  the  bite  of  a  rabid  dog,  the 
virus  remains  for  a  time  without  producing  either  local  or 
general  symptoms.  The  period  of  incubation  varies  withm 
quite  wide  limits.  The  virus  penetrates  the  nervous  system 
bv  following  the  nerve  trunks  from  the  site  of  infection  to  the 


466  RABIES 

spinal  cord,  then  through  the  spiual  cord  to  the  brain.  This 
has  been  proven  by  inoculating  an  animal  in  one  of  the  legs 
with  virulent  material.  After  a  suitable  time,  but  before  the 
symptoms  of  rabies  appear,  the  virus  will  be  found,  on  killing 
the  animal,  in  the  nerves  of  the  limb,  and  even  in  the  part  of 
the  spinal  cord  into  which  the  nerve  enters,  while  the  upper 
part  of  the  cord  and  the  brain  are  still  uninfected.  This  ex- 
plains the  fact  why  the  earliest  symptoms,  both  in  man  and 
animals,  such  as  itching,  tingling,  numbness  and  other  nerv- 
ous sensations,  often  appear  in  the  part  of  the  body  which  re- 
ceived the  virus.  In  the  case  of  a  bite  about  the  face  and 
head  the  route  along  the  nerve  to  the  central  nervous  system 
is  much  shorter.  While  the  nerves  seem  to  form  the  main 
route  by  which  the  virus  travels,  the  circulation  may  at  times 
assist,  especially  in  small  animals.  Inoculation  into  the  large 
nerve  of  the  leg  is  almost  as  certain  to  produce  the  disease,  as 
inoculation  directly  into  the  sub-dural  space,  while  injection 
beneath  the  skin  of  the  leg  is  not  so  sure.  Nicholl  finds  that 
the  virus  passes  from  the  point  of  infection  to  the  brain  ex- 
clusively through  the  nerves.  He  also  finds  that  it  is  rapidly 
destroyed  in  the  blood. 

Resistance  of  the  virus.  The  action  of  the  virus  is  de- 
stroyed b}'  drying  and  by  the  action  of  light.  In  dry  air,  pro- 
tected from  light  and  putrefaction,  the  virulence  of  the  spinal 
cord  of  rabbits  is  destroyed  in  fourteen  to  fifteen  days.  When 
spread  in  thin  layers  it  is  entirely  destroyed  by  drying  in  from 
four  to  five  days.  Sunlight  destroys  it  in  about  forty  hours. 
The  loss  of  virulence  by  drying  is  gradual  but  quite  regular, 
which  fact  was  taken  advantage  of  by  Pasteur  in  the  prepara- 
tion of  his  vaccine.  The  virus  may  be  preserved  in  neutral 
glycerin  at  ordinary  temperature  for  a  long  time.  Roux  found 
that  after  four  weeks  in  glycerin  at  30°  C. ,  the  virus  in  a  rabid 
brain  had  the  same  power  as  when  perfectly  fresh.  The  writer 
has  found  that  rabbits  inoculated  with  rabid  brains  that  had 
been  kept  in  glycerin  from  three  to  four  weeks  did  not  develop 
the  di.sease  as  quickly  as  those  that  were  inoculated  with  the 
freshly  removed  brain. 


PERIOD    OF    INCUBATION  467 

It  is  quite  resistant  to  putrefaction.  Galtier  found  the 
virus  active  in  the  central  nervous  system  of  rabbits  that  had 
been  buried  for  twenty-three  days,  of  sheep  buried  thirty-one 
days  and  of  dogs  buried  forty-four  days.  Other  observers  have 
found  it  still  active  in  animals  buried  for  twenty-four  days. 

It  is  destroyed  completely  by  a  temperature  oif  50°  C.  in 
one  hour  or  60°  C.  in  one-half  hour.  It  is  uninjured  by  ex- 
posure to  extreme  cold,  resisting  the  prolonged  application  of 
a  temperature  from  10  to  20°  C.  below  zero. 

Its  activity  is  destroyed  in  one  hour  by  a  five  per  cent, 
solution  of  carbolic  acid,  or  by  a  i  to  1,000  solution  of  corro- 
sive sublimate.  Water  saturated  with  iodine  destroys  it  in 
ten  minutes. 

§  371.  Period  of  incubation.  The  period  of  incuba- 
tion is  quite  variable,  depending  on  the  site  of  the  wound, 
whicli  is  almost  always  a  bite,  the  amount  of  virus  introduced 
and  its  virulence.  In  general  it  may  be  said  for  all  animals 
that  the  period  of  incubation  seldom  exceeds  sixty  days,  al- 
though in  man  and  in  some  larger  animals,  it  sometimes, 
though  very  rarely,  reaches  one  year.  A  few  cases  of  a  longer 
period  have  been  reported.  The  average  period  as  given  by 
Ravenel  is  as  follows  : 

In  man,  40  days. 

In  dogs,  21  to  40  days. 

In  horses,  28  to  56  days. 

In  cats,  14  to  28  days. 

In  pigs,  14  to  21  days. 

In  goats  and  sheep,  21  to  28  days. 

In  birds,  14  to  40  days. 

In  rabbits  inoculated  subdurally  with  the  brain  from  rabid 
animals,  the  writer  has  found  the  period  of  incubation  to  vary 
from  12  to  62  days  and  the  duration  of  the  disease  to  range 
from  a  few  hours  to  three  days.  Westbrook  reports  a  period 
of  incubation  in  rabbits  to  extend  in  one  case  over  a  hundred 
days.  In  the  disease  as  it  is  naturally  contracted  from  the 
bites  of  rabid   animals,   the  period  of  incubation  varies  with 


468  RABIES 

reference  to  the  location  and  extent  of  the  bites.  If  the  indi- 
vidual is  bitten  about  the  head  the  period  of  incubation  is 
much  shorter  than  if  the  injuries  are  on  the  extremities. 

In  the  dog,  the  period  of  incubation  in  144  cases  was 
clearly  determined  by  Peuch.  His  table  with  the  addition  of 
percentages  is  appended. 

PERIOD    OF    INCUBATION   OF    RABIES   IN    THE    DOG. 


Number  of  days  of 
incubation. 

Number   of 

cases. 

3 

Per  cent. 

5  to 

10 

2.0S 

10  to 

15 

8 

5-55 

15  to 

20 

13 

9-03 

20  to 

25 

25 

17.36 

25  to 

30 

13 

903 

30  to 

35 

25 

17-36 

35  to 

40 

6 

4.17 

40  to 

45 

II 

7-64 

45  to 

50 

9 

6.25 

50  to 

55 

4 

2.78 

55  to 

60 

2 

1-39 

60  to 

65 

7 

4.86 

65  to 

70 

I 

.69 

70  to 

75 

5 

3-47 

Soto 

90 

4.86 

100  to 

120 

4 

2.78 

365— 

tal 

.69 

Toi 

144 

The  somewhat  popular  opinion  that  most  of  the  cases  of 
rabies  occur  in  the  summer,  especially  in  "dog  days,"  is  not 
founded  upon  facts.  Rabid  dogs  are  nearly  if  not  quite  as 
numerous  in  winter  and  early  spring  as  in  summer.  Salmon 
has  collected  14,066  cases  of  rabies  in  dogs  with  the  months 
in  which  the  disease  occurred.  The  results  are  exceedingly 
interesting  as  the  appended  table  shows. 


SYMPTOMS  469 

CASES   OF    RAHIKS    IN    DOGS,    BV    MONTHS. 

^   ,     ~        -^   '    V.         >>        =         >■        M        a      ^   ^   s        i         "S 
Source  5,,^        g        ^        ?.         ^        — .        ^tcloSS        Q  H 

^^......89.55.53    .84    ;8,     -9    ;57    X47    ;33 -IjoS    Jg    ;6,. 

IsgS  ::::::  139    M8-      I8.^^_)85_i77_^-^^3_|54_i78i 
Total  .___  ^  ^  960  7^^  M^  1467  1435  1294  1 145  965  933  ii37  14066 

§  372  Symptoms.  Rabies  is  generally  divided  into 
two  forms,  furious  and  dumb.  In  the  first  the  animal  is  irri- 
table, aggressive  and  bites  nearly  every  object  which  comes  m 
its  way  •  in  the  second  the  muscles  of  its  jaws  are  paralyzed 
almost  from  the  beginning  and  being  unable  to  bite  the  ani- 
mal remains  more  quiet  and  tranquil.  Essentially  the  two 
forms  of  the  disease  are  the  same,  but  probably  owing  to  the 
parts  of  the  brain  attacked  or  the  acuteness  of  the  attack  or 
both  paralysis  appears  much  sooner  in  the  dumb  form  than  in 
the  other.  The  saliva  from  a  case  of  dumb  rabies  is  just  as 
dangerous  and  virulent  as  that  from  a  case  of  furious  rabies. 
Dogs  affected  with  dumb  rabies  are  less  dangerous  simply  be- 
cause thev  are  unable  to  bite  and  thus  to  infect  others. 

Dumb  rabies  and  furious  rabies  do  not  always  represent 
two  distinct  tvpes  of  disease.  The  typical  cases  belong  to  the 
two  extremes'of  symptoms  and  there  are  always  graduations 
between  them.  In  fact,  almost  every  case  of  furious  rabies 
sooner  or  later  changes  to  the  dumb  form,  that  is,  the  final 
stage  of  the  disease  is  almost  invariably  paralytic  In  the 
typical  development  of  the  dumb  form,  the  paralysis  occurs  on 
the  first  day  of  the  disease.  It  may  not  appear,  however, 
until  the  second  or  third  or  even  a  day  later. 

A-ain  a  dog  does  not  necessarily  bite  everything  about  it 
even  iflt  has  rabiesand  its  jaws  are  not  paralyzed.  It  may  be 
combative  and  furious  all  of  the  time  or  only  part  of  the  tune. 


470  RABIES 

or  not  at  all.  There  is  perhaps  no  other  disease  in  which  the 
symptoms  may  vary  more  than  in  rabies  of  the  dog. 

Furious  rabies.  The  symptoms  appear  very  gradually. 
The  animal's  habits  and  behavior  are  changed.  It  may  be 
more  restless  or  affectionate  than  usual,  seeking  to  be  near  its 
master  or  mistress,  fawning,  licking  the  hand  or  face  and 
apparently  seeking  sympathy  and  assistance.  Such  caresses 
are,  however,  extremely  dangerous,  for  the  animal's  tongue, 
moist  with  virulent  saliva,  coming  in  contact  with  a  part 
where  the  skin  is  thin,  abraded  or  wounded,  may  fatally  infect 
the  person  to  whom  it  is  endeavoring  to  demonstrate  its  affec- 
tion. The  reported  cases  in  which  rabies  have  developed  from 
such  inoculations  are  quite  numerous. 

In  most  cases  dogs  first  become  dull,  gloomy,  morose, 
seeking  solitude  and  isolation  in  out-of-the-way  places  or  retir- 
ing under  pieces  of  furniture.  But  in  their  retirement  they 
cannot  rest,  they  are  uneasy  and  agitated,  they  lie  down  and 
assume  the  attitude  of  repose,  but  in  a  few  minutes  they  are 
up  walking  about  "seeking  rest,  but  finding  none.""  Occa- 
sionally this  restlessness  may  disappear  for  a  time  and  the 
animal  becomes  lively  and  affectionate  ;  oftener  it  sinks  into  a 
sullen  gloominess  from  which  even  its  master's  voice  rouses  it 
but  temporarily.  At  this  period  dogs  may  have  aberrations  of 
the  senses  which  cause  hallucinations  and  lead  them  to  think 
they  are  being  annoyed  by  something  or  that  some  animal  or 
person  is  endeavoring  to  injure  them.  They  crouch  ready  to 
spring  upon  the  enemy  ;  they  rush  forward  and  snap  at  the 
air  ;  they  throw  themselves,  howling  and  furious,  against  the 
wall  as  though  they  heard  sounds  beyond  it. 

While  at  first  the  affected  dog  may  not  be  disposed  to  bite, 
it  becomes  more  dangerous  as  its  hallucinations  and  delirium 
increase. 

The  disturbance  of  the  sensations  leads  to  chills  and  itch- 
ing. If  the  place  where  the  bite  occurred  is  acces.sible,  the 
dog  licks  the  scar  and  later  may  bite  and  tear  the  tissues.  In 
this  case  it  bites  into  its  own  flesh  with  apparent  pleasure  and 
satisfaction.      Food  is  taken  at  first  if  it  is  something  that  can 


SYMPTOMS  471 

be  swallowed  without  mastication,  otherwise  it  is  soon  drop- 
ped. Difficulty  in  swallowing  is  an  early  symptom.  Mad 
dogs  have  no  fear  or  dread  of  water,  they  continue  to  drink 
until  paralysis  prevents  them  from  swallowing. 

When  the  furious  symptoms  appear,  the  dog  may  leave 
his  home  and  start  upon  a  long  chase  with  no  apparent  object 
in  view  other  than  to  be  traveling.  He  trots  at  a  rapid  pace, 
eyes  haggard  and  tail  depressed.  He  is  indifferent  to  the  sur- 
roundings. He  often  flies  at  and  bites  persons  whom  he 
meets,  but  usually  he  does  not  search  for  them  or  even  notice 
them  if  they  remain  quiet.  Dogs  in  this  condition  may  travel 
many  miles  and  finally  drop  from  exhaustion  and  die.  Often 
after  an  absence  of  a  day  or  two  they  return  to  their  homes, 
exhausted  and  emaciated,  presenting  a  most  forlorn  and  mis- 
erable appearance.  Those  who  have  pitj'  for  such  an  animal 
and  try  to  make  it  clean  and  comfortable  are  in  great  danger 
of  being  bitten,  as  the  di.sease  has  advanced  to  a  point  where 
the  delirium  or  insanity  is  most  marked  and  where  a  treacher- 
ous bite  is  most  common. 

If  the  animal,  instead  of  being  allowed  to  escape,  is  kept 
confined,  the  paroxysms  of  fury  are  seen  to  occur  intermit- 
tentl)'  or,  in  the  absence  of  provocation,  the}'  may  be  entirely 
wanting.  If  excited  it  howls,  rushes  upon  objects  that  are 
thrust  toward  it  or  throws  itself  against  the  bars  of  its  cage 
and  bites  with  great  fury. 

As  death  approaches  the  animal  becomes  exhausted  and 
is  .scarcely  able  to  stand.  The  eyes  are  dull  and  sunken  and 
the  expression  is  that  of  pain  and  despair.  Paralysis  appears 
in  the  jaws  or  in  the  posterior  extremities  and  extends  rapidly 
to  other  parts  of  the  body.  The  animal,  being  unable  to 
stand,  lies  extended  upon  its  side,  the  respiration  becoming 
more  and  more  difficult.  There  are  spasmodic  contractions  of 
certain  groups  of  mu.scles,  complete  prostration  and  finally 
death. 

The  usual  course  of  the  disease  is  four  or  five  days.  It 
may  be  as  short  as  two  or  as  long  as  ten  days. 

Dumb  rabies.     When  this  form  of  the  disease  is  typical,  it 


472  RABIES 

comes  on  with  restlessness,  depression,  a  teudencj^  to  lick 
objects  and  paralysis  of  the  muscles  which  close  the  jaws.  As 
a  consequence  of  the  paralysis,  the  lower  jaw  drops,  the 
animal  is  unable  to  close  the  mouth,  the  tongue  hangs  out  and 
an  abundance  of  saliva  escapes.  The  mucous  membrane  of 
the  mouth  becomes  dry,  discolored  and  covered  with  dust. 
The  animal  remains  quiet,  it  does  not  respond  to  calls  and 
appears  to  understand  its  helplessness.  Bouley  states  that  the 
animal  cannot  bite  and  does  not  desire  to  bite.  When  dumb 
rabies  follows  the  furious  form,  the  desire  and  tendency  to  bite 
may  be  retained  even  after  the  jaw  is  paralyzed. 

The  course  of  the  disease  is  short,  death  usually  occurring 
in  from  two  to  four  days. 

§  373.  Morbid  anatomy.  One  of  the  striking  charac- 
teristics of  rabies  is  the  absence  of  constant,  recognizable 
lesions.  The  mucosa  of  the  pharynx  and  larynx  are  con- 
gested. The  spleen  is  sometimes  enlarged  and  dark  colored. 
In  dogs  the  stomach  often  contains  a  variety  of  foreign  matter 
such  as  earth,  stones,  pieces  of  iron,  bits  of  leather,  wood,  etc. 
Axe  reports  finding  such  foreign  substances  present  in  90  per 
cent,  of  200  cases  he  examined.  Galtier  reports  such  findings 
in  from  50  to  70  per  cent.  In  experimental  animals  and  cattle 
the  writer  has  rarely  found  them.  It  seems  to  be  true  that 
the  obvious  lesions  are  not  constant  and  it  is  probable  that 
the  pronounced  changes  occasionall}^  found  in  a  single  organ 
are  accidental  or  secondary  rather  than  primarily  related  to 
the  disease.  The  lesions  in  the  brain  and  spinal  cord  are 
likewise  variable.  In  some  cases  there  is  a  marked  hyperemia, 
while  in  others  the  brain  appears  to  be  normal. 

Certain  investigators,  however,  have  found  histological 
changes  which  to  their  minds  have  been  pathognomonic  of  the 
disease.  The  close  simulation  of  the  nervous  lesions  to  those 
due  to  other  diseases,  and  the  possibility  of  greater  or  less 
post-mortem  changes  will  foster  an  element  of  doubt  in  the 
minds  of  the  majority  of  working  histologists.  This  doubt  in- 
stead of  diminishing  shows  a  tendencv  to  grow  when  a  review 


MORIUD    ANATOMY  473 

is  taken  of  the  conflicting  results  and  opinions  held  by  those 
who  have  already  inv^estigated  this  field.  It  also  appears  that 
some  portions  of  the  nervous  system  may  exhibit  lesions  of  a 
pronounced  character,  other  portions  very  slightly,  and  still 
others  none  at  all,  thus  presenting  additional  difficulties. 

One  of  the  most  common  lesions  that  has  been  observed  is 
of  an  inflammatory  character,  the  congested  blood  \essels  fre- 
quently showing  diapedesis  and,  according  to  some,  a  perivas- 
cular exudation  of  a  granular  or  a  hyaline  substance.  Hypere- 
mia and  lymph-stasis,  although  of  not  so  much  significance 
when  taken  by  themselves,  have  been  taken  into  consideration 
along  with  other  changes.  The  blood  vessels  quite  as  much 
or  even  more  than  the  nerve  structures  have  been  noted  as 
the  focus  of  some  of  the  most  marked  changes,  among  which 
are  the  proliferation  of  the  epithelial  cells  and  of  the  connect- 
ive tissue  elements  of  the  outer  coat,  with  the  infiltration  of 
lymphoid  cells.  Such  lesions  may  be  nodular  primarily,  but 
later  become  diffuse.  The  inflammatory  process  may  progress 
to  such  an  extent  as  to  obliterate  certain  vessels. 

Pathological  miliary  centers  have  been  noted  not  only  in 
the  axial  portions  of  the  nervous  system,  but  in  the  gray 
matter  as  well.  These  centers  were  formed  by  lymph  cells 
which  accumulate  notably  around  the  blood  vessels  T perivas- 
cular) and  the  nerve  cells  (pericellular)  as  well.  The  lesions, 
when  present,  are  observed  most  frequently  in  the  motor 
centers  of  the  oblongata  and  spinal  cord. 

The  following  observations  were  made  by  Babes,  in   1887  : 

1.  "In  animals  dead  from  street  rabies  there  are  found 
usually  a  hyperccmia  and  an  acute  generalized  oedema  of  the 
cerebral  meninges,  acute  hemorrhages  localized  around  certain 
vessels,  as  well  as  inflammatory  lesions.  On  microscope  exam- 
inations we  find  an  increase  of  the  plasma  cells,  augmentation 
of  the  reticular  substance,  fibrinous  in  character,  between  the 
several  layers  of  the  meninges. 

2.  "  The  epithelium  of  the  cerebrospinal  central  canal 
has    proliferated.      In   the   gray    matter   which   surrounds  the 


474  RABIES 

canal,  and  especially  in  that  of  the  floor,  hemorrhages,  some- 
times symmetrical,  are  often  found.  Microscopically,  we  often 
find  an  obliteration  or  thrombosis  of  a  vessel  by  a  reticulated, 
hyaline,  pigmented  material  or  by  leucocytes  or  hyaline  glob- 
ules, and  sometimes  a  hyaline  degeneration  or  even  inflamma- 
tion of  the  vascular  tunic.  The  extravasated  blood  also  con- 
tains much  of  the  hyaline  material.  The  hemorrhages  are 
often  limited  by  the  lymphatic  sheath  of  the  vessels.  At  the 
same  time  the  epithelium  of  the  ventricles  and  central  canal 
may  be  partially  lost.  This  last  is  occasionally  filled  with 
blood  or  plugs,  either  granular  or  hyaline  in  character. 

3.  "  With  the  naked  eye  small  centers  of  degeneration 
may  sometimes  be  noted  in  the  gray  matter,  but  often  they 
may  be  sought  for  in  vain. 

4.  "  The  most  constant  lesions  are  microscopic  in  char- 
ter ;  they  are  found  more  especially  in  the  gray  matter  sur- 
rounding the  cerebrospinal  canal  and  in  the  motor  centers  of 
the  medulla  and  spinal  cord.  These  lesions  consist  at  first  in 
hypersemia  and  accumulations  of  embryonic  cells  around  the 
small  vessels,  perithelial  or  migratory  in  origin,  often  showing 
indirect  division  ;  finally  there  are  also  found  lesions  of  nerve 
cells. 

5.  "  The  lesions  of  the  nervous  elements  of  the  parts  in- 
dicated is  quite  characteristic  ;  it  consists  of  signs  of  prolifera- 
tion, namely,  in  the  presence  of  several  small  cells  in  place  of 
one  large  one,  or  in  a  uniform  degeneration  and  often  in  the 
appearance  of  vacuoles  with  a  reduction  in  size  or  disappear- 
ance of  the  nucleus,  pr  again,  its  chromatic  network  disap- 
pears. These  cells  frequently  contain  pigment.  Round  uni- 
nuclear, more  rarely  multinuclear,  elements  of  a  lymphatic 
origin  often  invade  the  protoplasm  even  of  the  cell  and  fill  out 
the  dilated  pericellular  lymphatic  spaces  by  a  multiplication  ot 
small  nuclei. 

6.  "The  lesion  of  medullary  substance  is  less  pro- 
nounced, it  consists  chiefly  of  an  edema  of  the  medullary 
sheath  of  the  nerve  fibers. 


MORBID    ANATOMY  475 

7.  "In  certain  plasma  cells,  in  the  interior  of  and  around 
vessels,  sometimes  in  leucocytes,  in  lymphatic  spaces,  in  the 
altered  parts  of  certain  nerve  cells,  and  in  the  dilated  sheath 
of  nerve  fibers  may  be  seen  round  or  ameboid  granules  about 
I  A'  in  diameter,  pigmented  or  stainable  by  aniline  dyes,  and 
which  in  part  seem  to  possess  the  power  of  movement.  " 

More  recently  Babes  has  noted,  besides  the  lesions  above 
mentioned,  that  the  alteration  of  the  nerve  cells  is  usually 
accompanied  by  a  modification  of  their  protoplasmic  network 
and  concludes  that  "Whilst  admitting  that  the  lesions  of  rabies 
are  not  absolutely  characteristic,  and  that  it  may  be  that  in  a 
case  of  diffuse,  very  acute  myelitis  similar  lesions  may  be 
found,  it  is  necessary  all  the  same  to  state,  that  neither  in 
writing  nor  in  my  personal  experience  have  I  ever  met  with  a 
similar  case,  so  that  at  present  we  may  consider  the  lesion  ot 
rabies  as  characteristic.  In  other  infectious  diseases  there 
have  also  been  found  histological  lesions  characteristic  as  a 
whole,  although  composed  of  elements  not  absolutely  specific.'* 
Golgi  draws  attention  to  the  following  morbid  changes  in 
rabies  : 

(i)  Changes  in  the  structure  of  the  nucleus,  all  the  vari- 
ous phases  of  karyokinesis  may  be  simulated,  yet  no  true 
nuclear  division  may  take  place.  (2)  Changes  in  the  body  of 
the  cells,  such  as  vacuole  formation,  bladder-like  transforma- 
tion of  the  cells.  Changes  may  also  be  recognized  by  methods 
directed  to  the  study  of  the  outer  form  of  the  cell.  Here 
varicose  appearances  of  the  cell  processes  may  be  seen. 
Granular  fatty  changes  may  also  be  present.  An  important 
change  lies  in  the  displacement  of  the  nucleus.  The  periphery 
of  the  cell  becomes  homogeneous.  CUanular  fatty  changes 
are  also  seen  in  the  neuroglia  cells.  (3)  Changes  in  the  inter- 
vertebral ganglia.  The  author  would  look  upon  these  ana- 
tomico  pathological  changes  found  by  him  as  characteristic, 
while  here  not  only  the  sum  total  of  the  changes,  but  also 
their  order  of  occurrence  and  mutual  interdependence  are  taken 
into  consideration. 

The  morbid   process   is   parenchymatous  encephalo-myel- 


476  RABIES 

itis,  of  which  the  exact  exciting  cause  is  as  yet  unknown.  The 
changes  are  thus  grouped:  (i)  appearance  of  nuclear  chro- 
matin, peculiar  cell  division  (neuroglia  cells  and  vascular 
endothelium),  nuclear  movements  also  in  nerve  cells,  diffuse 
vascular  distension  and  leucocyte  infiltration,  revealing  a  con- 
dition of  irritation  ;  (2)  swelling,  vacuolation,  changes  of 
form,  granular  appearance  of  nerve  cells  and  neuroglia  ;  and 
(3)  more  advanced  changes  in  the  nerve  elements.  The 
changes  in  the  first  group  may  be  seen  as  early  as  five  days 
after  inoculation. 

In  a  more  recent  article  by  Germano  and  Capobianco  * 
attention  is  called  to  the  fact  that  the  destruction  of  some  of 
the  nerve  cells  in  rabid  animals  is  not  accepted  by  everybod)^ 
but  that  in  their  researches  they  have  been  able  to  confirm  the 
statements  made  by  Golgi,  that  instances  of  the  complete  dis- 
appearance of  nerve  cells  have  been  observed,  while  other  cells 
show  fatty  degeneration,  and  partial  destruction  of  the  irentirety 
represent  intermediate  stages  between  the  normal  cell  and  its 
total  disappearance.  The  alteration  of  the  nucleus  ma)^  pre- 
cede or  follow  that  of  the  cell  body. 

The  nerve  fibers,  either  in  the  white  or  gray  matter, 
undergo  a  certain  amount  of  change.  In  a  longitudinal  sec- 
tion of  the  myel,  especially  through  the  ventro-lateral  columns, 
there  are  noted  marked  changes  in  the  axis  cylinders.  In 
some  cases  they  appear  uniformly  swollen  for  their  whole 
length,  while  in  others  there  are  varicose  enlargements.  In 
the  swollen  portions  there  were  frequently  observed  small 
vacuoles  which  interrupted  the  continuity  of  the  axis  cylinder. 

During  the  year  1900,  the  discovery  of  changes  distinctive 
of  rabies  was  announced  by  Van  Gehucten  and  Nelis.  These 
changes  are  found  in  the  peripheral  ganglia  of  the  cerebro 
spinal  and  sympathetic  systems  and  are  especially  marked  in 
the  plexiform  ganglion  of  the  pneumogastric  nerve  and  the 
gasserian  ganglion.  Normally  these  ganglia  are  composed  of 
a  supporting  tissue  holding  in  its  meshes  the  nerve  cells,  each 
one  of  which  is  enclosed  in  a  capsule,  made  up  of  a  single 
layer  of  endothelial  cells.     The  action  of  the  rabic  virus  seems 


DIFFERENTIAL    DIAGNOSIS 


477 


to  exercise  its  effect  on  these  cells  particularly,  bringing  about 
an  abundant  multiplication  of  the  cells  forming  this  capsule, 
leading  finally  to  the  complete  destruction  of  the  normal  gang- 
lion cell  and  leaving  in  its  place  a  collection  of  round  cells. 
Ordinarily  a  considerable  number  of  ganglion  cells  will  be 
found  which  have  undergone  only  a  slight  change,  but  under 
certain  conditions  the  process  is  so  widespread  that  all  the 
ganglia  cells  are  destroyed.  The  intensity  of  these  changes 
varies  in  different  animals  ;  they  are  perhaps  most  pronounced 
in  the  dog,  less  marked  in  man  and  still  less  in  the  rabbit. 

Much  of  the  practical  value  of  these  findings  consists  in 
their  making  it  possible  to  make  a  sure  and  quick  diagnosis. 
It  is  possible  to  complete  the  examination  within  .six  hours 
after  the  death  of  the  animal,  and  under  ordinary  circum- 
stances a  positive  opinion  can  be  given  in  from  24  to  36  hours. 
It  is  important  that  the  animal  should  be  allowed  to  die,  and 
not  be  killed  prematurely,  as  where  the  disease  is  not  permitted 
to  run  its  full  course  ending  in  death,  the  changes  may  be 
absent  or  only  slightl}'^  developed. 

^  374.  Differential  diagnosis.  From  the  often  obscure 
manner  of  infection,  the  long  period  of  incubation,  the  varia- 
ble symptoms  and  the  absence  of  gross  morbid  changes  char- 
acteristic of  the  disease,  it  is  easy  to  mistake  rabies  for  various 
other  nervous  disorders  and  vice  versa,  unless  a  definite  method 
of  diagnosis  can  be  availed  of. 

Diaonosis  by  aiiimal  inoculation.  The  method  which  the 
experience  of  pathologists  has  shown  to  be  the  best,  is  the  sub- 
dural inoculation  of  rabbits  or  guinea-pigs  with  a  suspension 
of  the  brain  or  spinal  cord  of  the  suspected  animal.  The  sub- 
dural inoculation  with  the  brain  tissue  of  rabid  animals  was 
first  demonstrated  by  Pasteur  to  be  more  reliable  and  more 
rapid  in  its  results  than  the  subcutaneous  injections.  The 
procedure  is  simple.  The  brain  of  the  suspected  animal  is 
removed  with  aseptic  precautions  as  soon  as  possible  after 
death.  A  small  piece  of  the  brain  or  spinal  cord  is  placed  in  a 
sterile  mortar  and  thoroughly  ground  with  a   few  cubic  centi- 


478  RABIES 

meters  of  sterile  water  or  bouillon.  This  forms  the  suspension 
to  be  injected. 

The  hands  of  the  operator  and  all  instruments  are  care- 
fully disinfected.  The  rabbit  is  etherized,  the  hair  clipped 
from  the  head  between  the  eyes  and  ears,  and  the  skin 
thoroughly  washed  and  disinfected.  A  longitudinal  incision 
is  then  made,  the  skin  and  subcutaneous  tissue  held  back  by 
means  of  a  speculum,  a  crucial  incision  is  made  in  the  perios- 
teum on  one  side  of  the  median  line,  to  avoid  hemorrhage  from 
the  longitudinal  sinus,  and  the  four  parts  of  the  periosteum 
reflected  or  pushed  back.  By  the  aid  of  a  trephine  a  small 
button  of  bone  is  easily  removed  leaving  the  dura  mater 
exposed.  With  a  hypodermic  syringe  a  drop  or  more  of  the 
rabid  brain  suspension  is  injected  beneath  the  dura,  the  perios- 
teum is  replaced,  the  skin  carefully  sutured  and  disinfected 
and  the  rabbit  returned  to  its  cage.  As  soon  as  the  influence 
of  the  anesthetic*  has  passed  off  the  rabbit  shows  no  appear- 
ance of  discomfort.  If  the  operation  is  performed  in  the  fore- 
noon the  animal  partakes  of  its  evening  meal  with  the  usual 
relish.  The  inoculation  wound  heals  rapidly,  and  the  rabbit 
exhibits  every  appearance  of  being  in  perfect  health  until  the 
beginning  of  the  specific  symptoms,  which  occur  ordinarily  in 
from  fifteen  to  thirty  days  after  the  inoculation.  Occasionally 
the  symptoms  appear  earlier  than  fifteen  days  and  in  some 
cases  the  rabbits  are  not  attacked  for  from  one  to  three  months. 

The  symptoms  following  the  inoculation  are  quite  uni- 
form. There  is,  however,  a  marked  difference  in  the  length  of 
time  the  rabbits  live  after  the  initial  manifestation  ot  the  dis- 
ease. The  fact  should  be  clearly  stated  that  rabbits  do  not 
ordinarily  become  furious.  In  some  instances  they  are  some- 
what nervous  for  a  day  or  two  preceding  the  paralysis.  There 
appears  to  be  marked  hyperesthesia.  Usually  the  first  indica- 
tion of  the  disease  it  a  partial  parah^sis  of  one  or  both  hind 
limbs.     This  gradually  advances  until  the  rabbit  is  completely 

*Ether  should  be  used  in  preference  to  chloroform  for  rabbits,  as 
the  latter  frequently  causes  death,  while  the  former  can  be  administered 
with  comparative  safety. 


DIFFERENTIAL  DIAGNOSIS  479 

prostrated,  the  only  evidence  of  life  being  a  slight  respiratory 
movement.  The  head  occupies  different  positions.  In  some  it 
is  drawn  backward  as  in  tetanus  ;  in  others  it  is  drawn  down 
with  the  nose  near  the  fore  legs  ;  and  in  still  others  it  is 
extended  as  if  the  animal  were  .sleeping.  The  period  of  this 
complete  paralysis  varies  from  a  few  hours  to  a  few  days,  but 
ordinarily  it  does  not  exceed  twenty-four  hours.  Although 
these  animals  are  unable  to  move  voluntarily,  there  is  a  reflex 
action  of  the  limbs  until  a  very  short  time  before  death. 

During  the  period  of  incubation  the  temperature  of  the 
rabbit  is  normal.  As  the  time  approaches  for  the  first  symp- 
toms to  appear  there  is  an  elevation  of  temperature  of  from  i 
to  2  degrees,  which  continues  for  a  variable  length  of  time, 
but  rarely  longer  than  two  days.  This  is  followed  by  a  grad- 
ual or  usually  a  more  rapid  drop  to  the  subnormal,  which  con- 
tinues to  the  end. 

The  differential  diagnosis  in  experimental  animals  is  not 
difficult.  Rabbits  inoculated  with  several  varieties  of  patho- 
genic bacteria  frequently  exhibit  symptoms  of  paralysis  for  a 
brief  period  preceding  death.  In  cases  of  injury  to  the  brain 
or  spinal  cord  there  may  be  paralysis,  which  in  the  absence  of 
the  history  of  the  case  might  be  taken  for  that  of  rabies.  In 
these  cases,  however,  the  symptoms  appear  very  soon  after 
inoculation.  This  is  especially  true  when  the  paralysis  is  due 
to  mechanical  injury  of  the  brain  or  to  irritation  of  septic  sub- 
stances. In  the  case  of  the  pathogenic  bacteria  if  paralysis 
occurs  at  all  it  is  almost  invariably  preceded  by  marked  disa- 
bility. This  method  of  diagnosing  rabies  requires  that  the 
inoculated  animals  remain  apparently  well  for  a  considerable 
length  of  time  after  the  sul)dural  inoculation  and  before  the 
paralytic  symptoms  appear. 

The  lesions  found  on  the  post-mortem  examination  are 
also  of  much  assistance  in  making  a  diagnosis.  If  the  animal 
died  from  .septicemia  or  brain  injury  there  will  be  lesions 
almost  invariably  recognizable  in  the  brain  or  viscera.  In  the 
case  of  septicemia  a  bacteriological  examination  will  reveal  the 
presence  of    microorganisms.      If    the    death    was    caused    by 


48o 


:^^ 


..O- 

4*^- 


vi/% 


Fig.  III.  Section  of  a  normal 
plexiform ganglion  ;  {a)  and 
{b) ganglion  cells,  {c)  intercel- 
lular substance. 


rabies  the  inoculation  wound  in  the  head  should  be  healed 
perfectly,  there  should  be  no  abscess  and  the  menings  should 
be  free  from  exudates  and  the  brain  should  appear  perfectly 
normal,  except  that  in  rare  cases 
there  may  be  a  slight  injection 
of  the  blood  vessels.  The  viscera 
are  ordinarily  normal  in  appear- 
ance, with  possibly  the  exception 
of  the  liver,  which  we  have 
frequently  found  to  be  deeply 
reddened  and  the  gastric  mucosa, 
which  not  infrequently  shows 
dark  patches,  indications  of  dis- 
integrated hemorrhagic  areas.  A 
bacteriological  examination  fails 
to  reveal  the  presence  of  micro- 
organisms in  either  the  tissues 
or  blood.  Another  important 
point  which  has  been  noticed 
is  an  intense  rigor  mortis  fol- 
lowing death  from  rabies.  Kin- 
youn  states  that  this  was  a 
constant  feature  of  this  disease 
in  all  of  the  produced  cases 
which  have  come  under  his  ob- 
servation. Wesbrook  did  not 
observe  this  condition. 

Animals  other  than  rabbits 
have  been  used  and  a  number  of 
of  other  methods  of  inoculation 
have  been  proposed. 

Diagnosis  by  histological  cx- 
The  rapid  diagnosis  by  means 
of  the  histological  changes  pointed  out  by  VanGehuchten 
and  Nelis  has  been  very  successful  in  the  experience  of 
a  number  of  workers.  Ravenel  was  the  first  to  publish 
upon    this    method    in     this    country.      He    used     it     very 


'V 


^, 


Fig.  112.  Section  oj  plevi- 
fortn  ganglion  from  a  case  of 
rabies ;  {a) ganglion  cell,  (b) 
cells  infiltrating  the  ganglion 
cell  and  space. 

aminatioii    of  the  gatiglia. 


DIFKHRKNTIAL    DIAGNOSIS  4^1 

successfully  in  the  Laboratory  of  the  Pennsylvania  State  Live 
Stock  Sanitary  Board.  He  reported  its  use  in  52  cases.  We 
have  used  this  method  with  success. 

We  have  found  the  plexiform  ganglion,  which  is  situated 
just  outside  of  the  cranial  cavity  near  the  foramen  lacerum 
basis  cranii,  on  the  pneumogastric  nerve,  the  most  convenient 
and  the  most  desirable  for  study.  The  removal  of  this  gang- 
lion is  comparatively  easy  and  simple. 

There  are  two  ways  by  which  this  ganglion  can  be  easily  found  : 

1.  Take  up  the  pneumogastric  nerve  and  trace  it  anteriorly  to  the 
point  where  it  enters  the  cranium.  Near  this  point  a  slight  enlarge- 
ment, the  ganglion  of  the  trunk  of  the  vagus,  will  be  found. 

2.  Cut  through  the  skin  from  the  mandibular  symphysis  posteri- 
orly along  the  neck  and  reflect  it  back.  An  incision  is  then  made 
through  the  mylohyoid  muscle  near  the  inner  face  of  the  mandible 
posteriorly  past  the  digastric  muscle  and  superiorly  until  the  lingual 
nerve  going  to  the  tongue  is  exposed.  Trace  this  posteriorly  until  the 
point  where  it  enters  the  cranium  together  with  the  vagus  is  reached. 
In  this  way  it  is  easy  to  locate  the  vagus  nerve  and  the  plexiform  gang- 
lion. We  have  found  either  one  of  these  methods  or  a  combination  of 
the  two  very  convenient,  and  with  a  knowledge  of  the  location  of 
these  parts  there  is  no  reason  why  the  ganglion  should  not  be  removed 
quickly  and  easily. 

After  the  ganglion  is  removed  there  are  a  variety  of  methods  which 
may  be  used  in  fixation  and  staining.  The  following  we  have  found  to 
be  very  satisfactory.  As  soon  as  the  ganglion  is  removed  it  is  placed  in 
Flemming's  fluid  or  in  a  standard  aqueous  solution  of  mercuric  chloride 
for  a  few  hours,  washed  in  water,  carried  through  the  alcohols  and  sec- 
tioned by  the  paraffin  method.  With  this  method  of  fixation  it  is 
almost  imperative  that  the  sections  be  stained  with  iron  or  Dela- 
field's  hematoxylin,  of  which  we  have  found  the  latter  the  most 
convenient.  Alcohol,  either  95  per  cent,  or  absolute,  may  be  used  as  a 
fixer,  in  which  case  other  staining  methods  may  be  used.  However, 
the  fixation  by  this  method  is  not  as  good,  but  it  admits  of  a  trifle  more 
haste. 

Normally  this  ganglion  is  composed  of  a  fibrous  capsule  from  which 
a  supporting  fibrous  tissue  extends  into  the  interior,  holding  in  its 
meshes  the  nerve  cells,  each  of  which  is  enclosed  in  an  endothelial  cap- 
sule. The  changes  characteristic  of  rabies  consist  in  the  atrophy,  the 
invasion  and  the  destruction  of  the  ganglion  cell  as  a  result  of  new 
formed  cells,  evidently  from  the  endothelial  capsule.    These  cells  appear 


482  RABIES 

first  between  the  nerve  cell  and  its  capsule.  These  changes  are  quite 
uniform  through  the  entire  ganglion  and  in  advanced  cases  of  the  dis- 
ease nearly  all  of  the  nerve  cells  are  often  times  destroyed. 

Robineaux  examined  37  cases  that  died  of  rabies  with  positive  re- 
sults. In  animals  killed  during  the  course  of  the  disease  the  results 
varied.  In  40  such  cases,  he  found  the  lesions  in  11  and  they  were 
absent  in  29.  The  rapidity  with  which  ganglionic  changes  appear  seems 
to  vary  greatly  in  different  individuals. 

The  fact  must  be  kept  in  mind  that  this  is  a  method  for  rapid  diag- 
nosis in  case  the  animal  dies  and  not  a  means  for  an  early  diagnosis. 

Diagnosis  from  the  presentee  of  Negri  bodies.  The  presence 
or  absence  of  Negri's  bodies  is  used  as  a  means  of  diagnosis  in 
most  if  not  all  laboratories.  These  bodies,  which  are  often 
quite  large,  are  readily  brought  out  by  proper  staining.  These 
bodies,  whether  the  cause  or  specific  degenerations,  appear  to 
be  of  much  value  in  making  a  rapid  diagnosis.  Unlike  the 
ganglion  changes  they  appear  early  in  the  course  of  the  dis- 
ease, and  consequently  they  are  of  value  in  making  an  early 
diagnosis  when  the  animal  is  killed  soon  after  the  appearance 
of  the  first  symptoms.  Thus  far  these  bodies,  or  those  easily 
mistaken  for  them,  have  not  been  found  in  the  brains  of  ani- 
mals dying  from  other  diseases  except  one  report  of  their 
possible  presence  in  a  case  of  tetanus. 

Bohne  uses  for  diagnosis  of  rabies  a  piece  'j-rU  mm. 
thick  from  the  Ammons  horn  which  after  30-40  minutes  of 
fixing  and  hardening  in  aceton  for  60-75  minutes  he  puts  it  in 
paraffin.  In  this  way  it  is  possible  for  them  by  the  aid  of  a 
short  staining  after  the  Mann  method  to  get  stained  sections 
in  the  course  of  three  hours. 

In  his  170  investigations  (157  dogs,  6  cows,  4  people.  3 
cats)  he  found  the  later  discoveries  of  Negri  and  Volpino  con- 
firmed according  to  the  presence  of  the  Negri  bodies  and  their 
finer  structure. 

Besides  he  investigated  50  dogs  attacked  with  other  dis- 
eases without  finding  Negri  bodies  or  similar  forms.  He 
therefore  holds  the  Negri  bodies  as  specific  for  rabies  and  the 
diagnosis  as  assured  by  a  positive  find.  Their  parasitic  nature 
seems  to  him  for  the  present  still  doubtful. 


PREVENTION  483 

§  375.  Prevention  and  treatment.  The  prevention 
of  rabies  infection  resolves  itself  into  two  procedures,  (i) 
The  destruction  of  all  ownerless  and  vagrant  dogs,  and  (2)  the 
muzzling  of  all  dogs  that  appear  upon  the  streets  or  in  public 
places.  In  thus  preventing  the  propagation  of  the  virus,  as 
shown  by  the  results  obtained  in  German}-  and  Great  Britain, 
the  disease  will  be  practically  exterminated. 

There  is  no  treatment  for  rabies  except  the  preventive 
inoculation  known  as  the  Pasteur  treatment  by  which  an  im- 
munity is  produced  by  the  subcutaneous  injection  of  the  virus 
of  rabies  in  an  attenuated  form,  beginning  with  the  mildest 
virus  and  going  gradually  up  to  one  which  possesses  nearly  or 
full  virulence.  The  attenuation  of  the  virus  is  brought  about 
by  drying  at  a  fixed  temperature  and  the  action  of  the  atmos- 
phere. Depending  upon  the  length  of  time  the  virus  is  ex- 
posed to  the  influences,  we  can  obtain  any  degree  of  virulence 
desired,  the  loss  of  virulence  under  fixed  conditions  being 
quite  uniform. 

The  disease  as  seen  in  dogs  infected  naturally  was  called 
by  Pasteur  "street  rabies"  and  the  virus  of  such  animals  is 
known  as  the  "  virus  of  street  rabies."  Such  virus  will  as  a 
rule  produce  the  disease  in  rabbits  by  intra-cranial  inoculation 
in  from  three  to  four  weeks.  By  inoculating  rabbits  in  series 
one  from  the  other,  a  reduction  of  the  period  of  incubation  is 
obtained.  After  about  100  passages  rabbits  will  die  with  cer- 
tainty and  great  regularity  on  the  sixth  or  seventh  day  after 
inoculation.  Beyond  this  point  no  increase  of  virulence  has 
been  obtained.     This  is  the  fixed  virus  of  Pasteur. 

The  simultaneous  method  which  consists  in  the  injection 
simultaneously  of  a  strong  virus  and  the  serum  of  an  immune 
animal  is  now  being  used  with  reported  success  in  the  Pasteur 
Institute  of  Paris. 

RKFERKNCKS 

1.  Babks.  Sur  certains  caracteres  des  lesions  histoloijiques  de  la 
rage.     Ann.  dc  I'  Insiitui  Pasteur,  Vol.  \'I  (1892),  p.  299. 

2.  B.\BKS.     Untersuchungen  iiber  die  Negrischen  Korper  und  ilire 


484  RABIES 

Beziehung  zu  dem    Virus   der   Wutkrankheit.     Zeitschr.   f.    HygienCy 
Bd.  LVI  (1907),  S   435- 

3.  BOHNE.  Beitrag  zur  diagnostischen  Vervverthbarkeit  der  Negri- 
scheii  Korperchen.     Zeitschr.  f.  Hygiene,  Bd.  LII,  S.  87. 

4.  Cabot.  Report  on  experimental  work  on  the  dilution  method 
of  immunization  from  rabies.  Jour.  Experimental  Med.,  Vol.  IV 
(1899),  p    181. 

5.  Dulles.  Disorders  mistaken  for  hydrophobia.  Trans,  of  the 
Med.  Sac.  of  the  State  of  Penn.,  1884. 

6.  Fleming.     Rabies  and  hydrophobia. 

7.  FROTHINGH.A.M.  The  rapid  diagnosis  of  rabies.  Jour.  Med. 
Research. 

8.  Keirle.  a  report  on  the  autopsies  on  four  recent  cases  of 
rabies  and  a  bacteriological  examination  of  a  rabid  dog,  together  with 
the  recent  laboratorj'  experiments.  Maryland  Med.  Jour.,  Vol. 
XXXVIII  (1897). 

9.  Law.  Rabies.  A  System  of  Practical  Medicine  by  American 
Authors,  Vol.  Ill  (1898). 

10.  MacClure.  Rabies-hydrophobia.  Supplement  to  the  Annual 
Report  of  the  Michigan  Board  of  Health,  1894. 

11.  MoHLER.  Pathological  report  on  a  case  of  rabies  in  a  woman. 
Annual  Report,  U.  S.  Bureau  of  Animal  Industry,  1903,  p.  54- 

12.  Moore  and  Fish.  A  report  on  rabies  in  Washington,  D.  C. 
Annual  Report,  U.  S.  Bureau  of  Animal  Industry,  1895-6. 

13.  Moore  and  Way.  A  rapid  method  for  the  diagnosis  of 
Rabies.     American  Veterinary  Reviezv,  Oct.,  1904. 

14.  Negri.  Beitrag  zum  Studium  der  Aetiologie  der  ToUwuth. 
Zeit.  f  Hygiene,  Bd.  XLIII  (1903),  S.  507. 

15.  Poor.  Recent  studies  in  the  diagnosis  of  rabies.  Medical 
Record,  Apr.  15,  1905. 

16.  Public  Health  Commission,  District  of  Columbia. 
Rabies.     But.  25,  U.  S.  Bureau  of  Animal  Industry,  1900. 

17.  Ravenel  and  McCarthy.  The  rapid  diagnosi.-;  of  rabies. 
Univ.  of  Penn.  Med.  Magazine,  January ,  1901. 

18.  Ravenel.  Rabies.  Bui.  79,  Dept.  of  Agr.,  State  of  Penn., 
1901. 

19  RemlingER.  Le  passage  du  virus  rabique  a  travers  les  filtres. 
Ann.  de  I'  Inst.  Pasteur,  Vol.  XVII  (1903),  p.  834. 

20.  Remlinger  ET  RiffaT-Bev.  Sur  la  permeabilite  de  la  bougie 
Berkefeld  au  virus  rabique.     C.  R.  Soc.  de  Biol.,  Vol.  LV.  (1903)  p.  974- 


DIIMITHHRIA    IN    KOWI.S 


485 


SCHUDHR.     Der  Negrische  Erreger  der  Tolhvuth.     Deul.  Med. 


21.  Salmon.  Rabies,  its  cause,  frequency  and  treatment.  Year 
nook,  Dcpt.  of  Agriculture,  Washington,  D.  C.      1900. 

22.  Salmon.  Rabies  in  the  District  of  Columbia.  Circular  No. 
JO,  U.  S.  Bureau  of  Animal  Industry,  1900. 

23.  SirzOR.  Hydrophobia.  An  account  of  M.  I'asteurs  system. 
1887. 

24. 
Wochenschrift,  1903,  No.  39,  S.  700. 

25  VanGehuchtenandNelis  Diagnostic  histologique  de  la 
rage.     Annates  de  Med.  Vet.,  Vol.  XLIX  ( 1900).  p.  234. 

26.  WAV.  The  Negri  bodies  and  the  diagnosis  of  rabies.  Amer. 
Vet.  Review,  Vol.  XXIX  (1905^.  P-  937- 

27  WKSBROOK  AND  WiLSON.  Preliminary  report  on  the  labora- 
torydiagnosis  in  twenty  cases  of  suspected  rabies.  Trans.  Am.  Pubhc 
Health  Assn.,  1S9S. 

28.  Williams  and  Lowde.  The  etiology  and  diagnosis  of  hydro- 
phobia.   Jour,  of  Infectious  Diseases,  Vol.  3,  1905,  P-  452- 


DIPHTHERIA  IX  FOWLS. 

Synouxms.      Roup--,  pip;  canker;  swelled  head. 

§  376.  Characterization.  Diphtheria  of  birds  is  an  in- 
fectious disease  the  lesions  of  which  first  appear  on  the  mucous 
membrane  of  the  nasal  passages,  the  eyes,  the  mouth,  the 
pharvnx  and  larvnx,  and  which  may  extend  to  the  trachea, 
bronchi,  the  air  sacs,  the  intestines  and  possibly  to  other 
abdominal  organs.  The  disease  is  determined  by  a  grayish- 
yellow  fibrinous  exudate  which  forms  upon  the  mucous  surface 
of  one  or  more  of  the  parts  mentioned.  The  exudate  may  be 
so  abundant  as  to  obstruct  the  air  passages.  In  some  out- 
breaks, it  is  very  acute,  progres.ses  with  great  rapidity  and  de- 
stroys most  of  the  birds  attacked. 

'Fowls  (genns  Callus)  and  pigeons  (genus  Columba  )  are 
most  commonly  attacked  and  they  are  the  only  ones  considered 

*The  origin  of  this  term  is  somewhat  obscure,  but  it  is  supposed  to 
be  a  corruption  of  croup,  and  its  application  explained  on  account  of  a 
peculiar  hoarseness  accompanying  the  respiration  of  the  aftected  birds. 


486  DIPHTHERIA    IN    FOWLS 

in  this  discussion.  Avian  diphtheria  is  reported,  however,  to 
attack  turkeys,  ducks,  pea-fowls,  pigeons  and  pheasants.  It 
is  presumed  that  wild  birds  may  be  affected. 

Avian  diphtheria  is  quite  distinct  from  human  diphtheria. 
There  are  cases  on  record,  however,  which  indicate  that  the 
diphtheria  of  fowls  may  be  communicated  to  children  and 
cause  a  serious  and  even  fatal  sore  throat.  On  the  other  hand, 
it  is  asserted  that  diphtheria  of  children  is  sometimes  com- 
municated to  fowls  and  that  the  virus  may  be  thus  preserved 
for  a  considerable  time  and  again  be  transmitted  to  children. 
Concerning  this  point  additional  investigations  are  needed. 

§  377.  History.  The  history  of  this  disease  is  some- 
what obscure.  It  is  evident  from  the  literature,  that  fowls 
have  always  been  subject  to  various  affections  of  the  head  but 
the  first  investigation  of  this  class  of  maladies  seems  to  have 
been  made  by  Loeffler-'^  in  1884.  Since  that  time  Klemmeri", 
Babes  and  Puscarin +,  Eberlin  ||,  Loir  and  Ducloux*,  and 
others  have  studied  diseases  known  as  diphtheria  in  pigeons, 
fowls  and  other  birds.  The  disease  was  investigated  by  the 
Bureau  of  Animal  Industry  in  1893-4.  It  has  more  recently 
been  studied  in  California  by  Ward,  in  New  York  by  Mack, 
and  at  Guelph,  Ontario,  by  Harrison  and  Streit. 

§  378.  Etiology.  In  1884,  Loeffler  discovered  a  bac- 
terium which  he  believed  to  be  the  specific  cause  of  diphtheria 
in  fowls  and  with  which  he  could  produce  the  disease.  It 
differed  from  the  diphtheria  bacterium  in  man.  Loir  and 
Ducloux  isolated  a  still  different  organism.  The  writer  found 
in  the  exudates  of  the  earlier  stages  of  the  disease  a  bacterium 
belonging  to  the  septicemia  hemorrhagica  group.  It  was 
rapidly  fatal  to  rabbits  but  the  diphtheritic  lesions  could  not  be 
produced  by  inoculation  in  fowls.     In  the  examinations  of  the 


*Mitt.  aus  dem  Kaiserlichen  Gesundheitsamte.  Bd.  II  ( 1884),  S.  214. 
tBerliner  theirarzt.  Wochenschrift.     1890,  No.  ib,  S.    138. 
jZeitschrift  f.  Hygiene.     Bd.  VIII  (1890),  S.  374. 
IIMonatshefte  f.  Thierheilkunde.     Bd.  V  (1894),  S.  433- 
lAnn.  de  I'Inst.  Pasteur.     Tome  VIII  (1894),  p.  599. 


ETIOLOGY 


4S7 


last  three  years  this  organism  has  not  been  found  in  the  diph- 
theritic lesions  of  fowls.  King  found  a  bacterium  on  the  con- 
junctiva of  a  healthy  fowl  that  belongs  to  this  group.  Ward 
failed  to  find  it  in  his  study  of  the  disease  in  California.  Har- 
rison and  Streit  have  described  an  organism,  Bacillus  cacosmus, 
which  they  consider  specific.  Ps.  pyocyaiieus  has  also  been 
obtained  in  pure  culture  from  the  exudates.  Mack,  who  has 
made  a  careful  study  of  this  disease,   has  failed  to  find  anv 


Fig.  113.       Fowl  shorving  eye  closed.      The  conjunctiva  is  covered  uitk 
a  tliick  exudate  (  Ward). 

organism  constantly  present  in  the  lesions.  He  also  failed  to 
produce  the  disease  with  />.  cacosmus.  It  is  not  positive,  how- 
ever, that  the  same  di.sease  was  studied  by  the  different  writers. 
Roup  is  usually  introduced  into  a  flock  by  the  exposure 
of  the  birds  to  sick  ones  at  shows  or  by  bringing  affected  fowls 
on  the  premises.  The  contagion  may  be  carried  by  birds 
which   have   the   disease  in  .so  mild  a  form  tliat  thev  show  no 


488  DIPHTHERIA    IN    FOWLS 

symptoms  of  it.  There  is  a  general  belief  that  the  disease  ma}- 
be  developed  by  exposure  of  birds  to  draughts  of  air  or  b}^ 
keeping  them  in  damp,  filthy  and  badly-ventilated  houses. 
It  is  presumable  that  this  belief  in  its  etiology  is  not  well 
founded  because  of  confusion  existing  concerning  the  early 
symptoms  of  acute  diphtheria  and  those  of  all  stages  of  the 
chronic  form,  and  those  of  simple  colds  and  catarrhs.  Ward 
was  unable  to  produce  the  disease  by  exposing  fowls  to  unfa- 
vorable  conditions,  but  when  infected  fowls  were    introduced 


Fig.  114.     Fo^i'l  s/i07tniig-  the  suborbital  sinus  distended.     T/ie  eye  is 
partially  closed. 

the  disease  spread  rapidly.  Dampness  and  lack  of  ventilation 
110  doubt  favor  the  maintenance  of  the  virus  when  introduced. 

The  specific  cause  of  the  disease  known  as  diphtheria  or 
roup  in  chickens  and  pigeons,  in  the  opinion  of  the  writer,  is 
not  known.  It  is  not  impossible  that  a  number  of  organisms 
may  share  in  the  production  of  the  lesions  of  this  affection. 

Guerin  considers  it  a  general  disease  caused  by  a  cocco- 
bacillus  (resembling  the  fowl  cholera  organism).  This  is  not 
unlike   the   bacterium  of  septicemia  hemorrhagica.      He  finds 


SVMl'TOM^ 


4«9 


it  in   the  blood   and   organs.      Moore,    Mack  and   Ward  have 
failed  to  find  this  organism  in  the  tissues. 

^  379-  Symptoms.  There  is  a  watery  secretion  from 
the  nostrils  and  often  from  the  eyes,  with  general  weakness 
and  prostration  greater  than  would  be  expected  from  snnple 
catarrh  The  birds  sit  with  the  back  arched,  the  head  and 
neck  drawn  out  towards  the  body,  the  plumage  roughened  ; 
the  respiration  is  more  or  less  obstructed,  rapid  and  audible, 
the   vision   is  impaired  and  swallowing  is  difficult.     There  is 


"Li' 


Pt 


Fig.  115.   /uu'/y  sfa.Qrs  of  diphtheritic  necrosis  in  the  throat  of  a  pi-eon. 

frequent  shaking  of  the  head,  sneezing  and  expectoration  of 
mucous  secretions.  If  the  mouth  is  examined  at  this  early 
period  the  tongue  is  found  to  be  pale,  while  small  grayish 
spots  shaded  with  black  and  slightly  projecting  above  the 
surface,  may  be  seen  along  the  border,  the  upper  surface  or  at 

the  base. 

The  following  day  the  condition  is  aggravated,  the  tem- 
perature is  several  degrees  above  normal,  the  appetite  has  dis- 
appeared and  there  is  diarrhea  with  greenish  or  yellowish 
evacuations.  From  the  open  beak  there  escapes  a  thick, 
strino-v  grayish  mucus.  The  eyes  are  unnaturally  dilated, 
projecting  and  possibly  partly  covered  with  the  thick  secretion 
which  has  accumulated  between  the  lids.  The  nostrils  are 
obstructed  by  the  thickened  and  dried  secretion.      W  alking  is 


490  DIPHTHERIA    IN    FOWLS 

irregular  and  difficult.  The  mucous  membrane  of  the  mouth 
and  pharynx  is  congested  and  shows  numerous  dark  red  eleva- 
tions covered  with  fibrinous  exudate.  The  patches  on  the 
tongue  have  increased  in  size,  the}'  are  gray  in  color,  dried 
along  the  edges  of  the  tongue  but  soft  and  flattened  upon  its 
upper  surface.  They  are  covered  with  membranous  deposits. 
The  voice  often  fails. 

§  380.      Morbid  anatomy.     The  lesions  are  largely  local- 
ized on  the  mucosa  of  the  head.      With  tlie  exception  of  ema- 


Pmu. 


■W'lyy 


Fig.  116.  A  section  through  a  diphtheritic  exudate,  late  in  the  course  of 
the  disease,  from  a  pigeou's  throat. 

ciation,  there  are  no  lesions  or  evidence  of  organic  disease. 
The  cause  of  death  and  the  extreme  emaciation  are  difficult  to 
explain  in  those  cases  where  the  lesions  are  confined  to  one 
eye  or  to  the  mucosa  of  the  nares,  excepting  on  the  supposi- 
tion that  some  poisonous  or  toxic  substance  was  absorbed 
from  the  seat  of  the  disease.  In  those  cases  where  the  lesions 
are  in  both  eyes,  or  in  the  mouth  and  throat,  difficulty  in  find- 
ing or  swallowing  food  affords  a  rational  explanation. 

In  some  cases  the  exudate  is  of  a  croupous  character,  in 
others  of  a  diphtheric  nature.  Three  stages  or  varieties  of 
lesions,    which    represent    the    types   of    this    disease    as    en- 


MORBID    ANATOMY  491 

countered  in  this  country,  may  be  more   definitely   defined   as 
follows  : 

1.  An  exudate  of  a  serous  or  muco-purulent  character  in 
the  conjunctiva  and  nasal  cavities.  Ordinarily  this  condition 
cannot  be  recognized  in  the  mouth.  The  mucosa  in  these 
cases  is  apparently  but  slightly  altered. 

2.  The  mucosa  over  a  small  or  larger  area  is  covered 
with  a  spreading  exudate  of  a  grayish  or  yellowish  color.  It 
is  firmly  attached  to  the  mucous  membrane  and  when  removed 
leaves  a  raw,  bleeding  surface.  Sections  through  this  exudate 
and  the  subjacent  tissues  show  that  the  epithelial  layer  is  de- 
stroyed and  the  underlying  tissue  infiltrated  with  cells.  The 
extent  of  the  infiltration  varies  in  different  individuals. 

3.  The  mucosa  is  covered  with  a  thick  mass  of  exudate, 
varying  in  color  from  a  milky  white  to  a  lemon  yellow  or 
brown.  It  is  easily  removed,  leaving  a  more  or  less  granular 
and  healed  surface.  This  sloughed  mass  is  frequently  dried  at 
its  margins  to  the  adjacent  tissue.  It  emits  a  strong  putrid 
odor,  due  to  decomposition.  The  drying  of  the  margins  pre- 
vents the  fowl  from  expelling  the  exudate  after  it  becomes 
separated  from  the  underlying  tissue. 

The  evidence  to  support  the  supposition  that  the  three 
forms  or  types  of  exudate  described  are  different  stages  in  the 
same  morbid  process,  as  gathered  from  the  post-mortem  notes 
and  bacteriological  study  of  the  cases  investigated,  may  be 
summarized  as  follows  : 

(a)  Abnormal  conditions,  representing  the  intermediate 
and  connecting  links  between  the  types  of  lesions,  are  fre- 
{{uently  encountered. 

(/')  Although  at  the  time  of  examination  (post-mortem) 
but  one  form  of  exudate  is  usually  present  in  a  single  fowl, 
there  are  exceptions,  in  which  two  and  occasionally  the  three 
forms  are  coincident.  Thus  the  eye  is  covered  with  a  sloughed 
exudate,  the  posterior  nares  contains  a  layer  of  muco-purulent 
substance  and  on  the  mucosa  of  the  mouth  are  areas  of  diph- 
theritic exudate. 


,|TY 


) 


492 


DIPHTHERIA    IN    FOWLS 


In  fowls  which  die,  the  exudates  are  for  the  greater  part 
in  the  advanced  stage,  although  fatal  cases  occur  in  which  the 
lesions  are  restricted  to  an  abnormal  quantity  of  a  serous  or 
muco-purulent,  more  or  less  viscid,  exudate  in  the  conjunctiva 
or  nasal  cavities.  The  best  illustration  of  the  diphtheritic 
process  is  found  in  fowls  killed  for  ex- 
amination in  the  second  stage  of  the 
disease.  The  distribution  of  the  lesions 
shows  that  the  conjunctiva  is  most  fre- 
quently affected.  The  exudate  in  the 
nasal  cavities  is  in  some  cases  undoubt- 
edly the  result  of  the  coagulation  of  the 
liquid  which  has  passed  during  the 
course  of  the  first  stage  from  the  con- 
junctiva through  the  lachrymal  duct  into 
the  nares.  In  certain  cases,  however, 
the  lesions  appear  in  the  nares  primarily. 
In  some  cases  the  exudate  appears  in  the 
larynx  and  extends  down  into  the 
trachea.  In  these  cases  the  fowls  are 
liable  to  die  from  suffocation.  It  occa- 
sionally happens  that  the  lesions  are 
restricted  to  the  larynx  and  as  the  fowls 
die  suddenly  the  cause  of  death  is  not 
suspected.  Sections  of  the  exudate  with 
subjacent  tissues  from  the  cornea  and  the 
mouth,  show  that  there  is  a  cell  infiltration  into  the  mucosa 
which  destroys  the  epithelial  layer  and  frequently  the  sub- 
mucous tissues  to  a  considerable  depth. 

The  fact  should  not  be  overlooked  that  the  disease  in  the 
eye  is  usually  confined  to  the  conjunctiva  and  the  cornea,  the 
posterior  portion  remaining  apparently  normal. 

Mack  in  his  work  on  thirty-three  cases  found  40  per  cent 
had  lesions  in  the  conjunctiva  ;  in  44  per  cent  the  nasal 
mucosa  was  affected  ;  in  41  per  cent  the  mouth  was  invoh^ed 
and  in  33  per  cent  the  suborbital  sinuses  were  distended  with 
exudates. 


Fig.  117.  A  drazviuo- 
shoii'ing  areas  of  diph- 
theritic e.vudate  in  the 
throat  of  a  pigeon. 


MOKHID    ANATOMY  493 

From  the  observations  thus  far  made  the  provisonal 
theory  is  entertained  that  the  three  forms  of  the  exudate — 
serous  or  muco-purulent,  diphtheritic  and  sloughed  mass- 
represent  three  stages  in  the  course  of  the  same  disease.  It  is 
easily  understood  that  fowls  examined  in  the  first  stage  would 
be  said  to  be  affected  with  a  catarrhal  condition  of  the  mucosae 
of  the  eyes  or  nares.  It  is  highly  probable  that  in  many  cases 
the  disease  never  reaches  the  second  stage  and  if  these  cases 
alone  were  examined  the  diphtheritic  condition   would   not   be 

^■iJMik-^::  (X  M 


'W^^^:^-'0' 


•  -^"^  Fig.   119.     A  longitudinal  sec- 

FiG.    118.      Dip/it /untie    e.vu-  Hon   through   the  larynx  and 

date  in  the  larynx  of  a  fowl :  trachea  of  a  fowl  {same  as  118) , 

(a)  the  grayish-white  exudate  showing  the  exudate:  («)  in  the 

projecting  from  the  glottis.  larynx  and  (b)  in  the  trachea. 

suspected.  It  appears,  however,  that  in  the  majority  of  cases 
the  disease  runs  its  course  and  membranes  are  formed,  slough 
and  recovery  follows.  It  is  furthermore  presumable  that  the 
disease  in  que.stion  appears  sometimes  in  a  virulent  and  de- 
structive form.  I  am  in  possession  of  statements  from  poultry 
raisers  which  show  that  there  are  occasionally  epizootics  of  a 
disease  characterized  by  exudates  in  the  eyes,  nose  or   mouth. 


494  DIPHTHERIA    IN    FOWLS 

which  run  a  rapidly  fatal  course.  It  appears  that  it  is  such 
outbreaks  which  have  been  reported  in  Europe  as  diphtheria 
and  not  the  low  form  of  chronic  inflammation  which  has  been 
studied  in  this  country. 

§  381.  Differential  diagnosis.  The  differential  diag- 
nosis of  diphtheria  in  fowls  cannot  be  made  until  we  are  pos- 
sessed of  a  knowledge  of  its  cause.  At  present  all  affections 
of  the  head  characterized  by  the  range  of  lesions  admitted  by 
the  description  of  the  morbid  anatomy  are  accepted  as  cases  of 
diphtheria  or  roup.  Chicken  pox  is  separated  by  the  nodular 
character  of  the  lesions.  Manson's  eye  worm  (oxyspirura 
Mansoni)  of  chickens  produces  lesions  that  might  be  mistaken 
for  roup.  The  finding  of  this  worm  would  determine  the 
diagnosis. 

§  382.  Relation  of  diphtheria  in  man  to  that  in  fowls. 
A  comparison  of  the  bacillus  of  diphtheria  in  man  (Klebs- 
Loeffler)  with  those  described  from  diphtheria  in  fowls  shows 
that  morphologically  and  in  their  pathogenesis  for  experimen- 
tal animals  the  organisms  are  in  no  way  alike.  There  is  also 
a  marked  difference  in  the  nature  of  the  exudates  in  fowls  and 
in  man.  The  non-identity  of  these  diseases  has  been  clearly 
pointed  out  by  Menard.*  Although  these  maladies  are  shown 
by  several  observers  to  be  unlike  in  their  etiology  and  the 
character  of  their  lesions,  the  transmission  of  fowl  diphtheria 
to  the  human  species,  and  vice  versa,  is  affirmed  by  several 
writers. 

Gerhardt  reports  4  cases  of  diphtheria  in  Wesselhausen, 
Baden,  among  6  workmen  who  had  charge  of  several  thousand 
fowls,  many  of  which  died  of  diphtheria.  There  were  no 
other  cases  of  diphtheria  in  the  neighborhood  and  the  evidence 
was  quite  conclusive  that  the  disease  was  contracted  from  the 
affected  fowls. 

Debrie:{:  reports  briefly  the  transmission   of   human   diph- 


*Revue  d'Hygiene.     Tome  XII  (1890),  p.  410. 

t  Reviewed   in   Centralblatt   f.     Bakteriologie.       Bd.    XIII    (1893), 
S.  730. 


PKKVKNTION  495 

theria  to  fowls.  He  is  inclined  to  the  view  that  human  diph- 
theria is  transniissable  to  fowls  and  fowl  diphtheria  to  man. 
Cole*  reports  a  case  of  supposed  transmission  of  the  disease 
from  a  fowl  to  a  child. 

The  diphtheritic  disease  of  fowls  reported  by  Loir  and 
Ducloux  in  Tunis,  in  1894.  spread  to  the  people  of  that  place, 
resulting  in  an  epidemic  of  serious  proportions.  Menard  re- 
fers to  the  fact  that  men  employed  to  feed  young  squabs  con- 
tracted diphtheria  by  blowing  the  masticated  food  into  the 
mouth  and  crop  of  squabs  suffering  with  that  disease.  vSchrev- 
enst  reports  several  cases  of  diphtheria  in  children  in  which 
he  traces  the  source  of  infection  to  certain  poultry. 

Guerin  has  pointed  out  with  emphasis  that  there  is  no  re- 
lation between  diphtheria  in  man  and  in  fowls. 

Although  the  number  of  reported  cases  of  the  transmission 
of  fowl  diphtheria  to  the  human  species  and  vice  versa  is  small 
in  comparison  with  the  extent  of  the  disease  in  poultry,  the 
evidence  that  such  a  transmission  is  possible  is  quite  sufficient 
to  discourage  the  careless  handling  of  diseased  fowls.  It  is  a 
quite  common  practice,  especially  in  the  rural  districts,  to 
bring  the  sick  chickens  into  the  house  for  treatment,  where 
the  children  of  the  household  are  allowed  to  fondle  them  at 
will.  It  is  not  improbable  that  when  this  disea.se  is  thorough- 
ly investigated  the  number  of  cases  of  direct  infection  from 
this  source  will  be  found  to  be  much  less  than  it  is  at  present 
supposed.  Until  such  investigations  are  satisfactorily  com- 
pleted the  indiscriminate  handling  of  diphtheritic  chickens  es- 
pecially by  children  and  the  exposure  of  fowls  to  the  infection 
of  diphtheria  in  the  human  species,  whereby  they  may  become 
carriers  of  the  virus,  should  be  strenuously  avoided. 

;<  383.  Prevention.  In  order  to  prevent  this  disease  it 
is  evident  that  many  conditions  must  be  strictly  complied 
with.     The  character  of  the  food  and  the  general  sanitary  cou- 


*  Archives  of  Pediatrics,  XI  {1894),  p.  38 
II  Bulletin 
(1894),  p.  380- 


II  Bulletin  de  1'  Acad.    Royale   de   M^d.    de    Helgique.    Vol.    \III 


496 


DIPHTHERIA    IN    FOWLS 


6 


Fig.  I20.     Scciions  of  the  heads  of  a  normal  and  of  a  diphtheritic  foivl. 


PREVENTION  497 

ditions,  including  cleanliness,  ventilation  and  the  temperature 
of  the  poultry  houses,  must  be  considered.  Undoubtedly  there 
is  much  to  be  learned  in  connection  with  the  proper  sanitary 
care  of  poultry.  In  addition  to  the  general  sanitary  methods, 
the  following  rules  should  be  observed. 

1.  Fowls  which  have  an  exudate  on  any  of  the  mucous 
membranes  of  the  head  or  which  have  come  from  flocks  in 
which  such  a  disease  exists  or  has  recently  existed,  .should  not 
be  placed  among  healthy  poultry. 

2.  If  the  disease  appears  in  one  or  more  fowls  of  a  flock 
they  should  be  immediately  separated  from  the  well  ones.      If 


Fig.  I20.     Photographs  of  transections  of  fowl's  head. 
I,  2  and  3.     Sections  from  a  normal  head. 

4,  5  and  6.  Sections  from  approximately  corresponding  levels  from 
the  heads  of  fowls  suffering  with  diphtheria. 

1.  Cross-section  of  a  chicken's  head  just  posterior  to  the  nasal 
openings,  a  Nasal  passage,  b  turbinated  bone,  c  portion  of  the  wall  of 
the  false  nostril,  d  sub-orbital  sinus,  e  palate. 

2.  Cross-section  of  a  chicken's  head  midway  between  the  nasal 
openings  and  the  eyes,  d  Sub-orbital  sinus,  </'  superior  portion  of  the 
sub-orbital  sinus,  which  connects  with  d  posterior  to  the  lachrymal 
duct,/  lachrymal  duct  opening  into  the  mouth  through  the  cleft  palate. 

3.  Cross  section  of  a  chicken's  head  on  a  level  with  the  anterior 
part  of  the  eyes,  d  Sub-orbital  sinus  and  the  duct  connecting  it  with 
the  nares. 

4.  Cross-section  of  a  chicken's  head  just  posterior  to  the  nasal 
openings,  showing  the  swollen  condition  of  the  nasal  mucosa  in  the  first 
stage  of  the  disease.  The  nasal  passages  are  nearly  occluded,  h  Tur- 
binated bone  with  swollen  mucosa,  d'  sub-orbital  sinus  containing  a 
small  amount  of  exudate. 

5.  Cross-section  of  a  chicken's  head  midway  between  the  nasal 
openings  and  the  eyes,  showing  extensive  exudate  in  the  left  sub- 
orbital sinus  d  and  nasal  passage  extending  into  the  cleft  palate  ;«. 
The  exudate  is  crowding  upon  the  turbinated  bones  and  nasal  septum. 

6.  Cross-section  of  a  chicken's  head  through  the  eyes,  showing 
exudate  in  the  conjunctival  sac,  inflammatory  thickening  of  the  eyelids 
and  membrana  nictitans,  and  ulcerated  cornea,  a'  Kyelid,  //  membrana 
nictitans,  i  exudate  in  the  conjunctival  sac,  k  ulcerated  cornea,  /eye. 

All  sections  are  magnified  two  diameters. 


49^  DIPHTHERIA    IX    FOWLS 

possible,  the  source  of  the  infection  should  be  determined  and 
removed. 

3.  The  quite  common  practice  of  allowing  fowls  from 
different  flocks  to  run  together  during  the  day  should  be  dis- 
couraged. 

4.  Care  should  be  taken  to  avoid  the  possibility  of  bring- 
ing the  virus  of  the  disease  from  affected  flocks  in  the  dirt  or 
excrement  which  naturally  adheres  to  the  shoes  in  walking 
through  an  infected  chicken  yard.  The  same  care  is  necessary 
in  the  interchange  of  working  implements,  such  as  shovels, 
hoes  and  the  like. 

Ward  has  found  that  this  disease  can  be  prevented  by 
keeping  infected  fowls  away. 

It  is  evident  to  any  careful  observer  that  the  fact  is  too 
often  overlooked  that  fowls,  owing  to  their  method  of  living, 
are  more  liable  to  infection  than  other  farm  animals.  This  is 
especially  true  when  they  are  allowed  to  run  at  random,  pick- 
ing their  living  from  the  garbage  pile  and  barnyards,  or  secur- 
ing even  more  unwholesome  food.  There  is  little  doubt  that 
many  so  called  outbreaks  of  contagious  disease  among  fowls  are 
simply  enzootics  brought  about  by  various  infections  to  which 
they  have  been  exposed. 

The  wide  distribution,  the  large  niimber  of  fowls  affected 
and  the  usual  chronic  course  of  this  disease  render  it  one  of 
the  few  poultry  affections  for  which  curative  measures  promise 
to  be  of  some  practical  value.  The  most  certain  of  the  known 
methods  of  treatment  is  the  local  application  of  disinfectants, 
among  which  a  weak  solution  of  carbolic  acid  appears  to  be 
the  most  satisfactory.  The  dipping  of  the  heads  of  fowls  in  a 
solution  of  I  to  2  per  cent  of  permanganate  of  potash,  or  a  3 
per  cent  solution  of  creolin  is  reported  to  be  very  effective  in 
cases  where  the  lesions  are  external  and  in  the  early  stages. 
The  fact  that  the  lesions  are  so  much  exposed  renders  the  dis- 
ease especially  favorable  for  topical  applications.  When  the 
exudates  are  in  the  suborbital  sinus  or  in  the  nares  there  is 
less  opportunity  for  treatment. 


INFLUENZA  499 

REFEREN'CKS. 

1.  GuERiN.  Siir  la  non-identite  de  la  diphtherie  humaine  et  de  la 
diphtheric.     Recueil  de  Med.  VH.,  1903,  p.  20. 

2.  Gratia  et  LiEnaux.  Contributions  a  I'ctude  bacteriologique 
de  la  diphterie.     Annales  de  Med.  Vet.,  Vol.  XLVII  (189S),  p.  401. 

3.  Harrison  and  Streit.  Roup.  Am.  Vet.  Review,  Vol.  XXVH 
(1903),  p.  26. 

4.  Harrison  and  Streit.  Roup  :  An  experimental  study.  lUil- 
letin  132.     Ontario  A,q-ric.  Coll.  and  Exp.  Farm,  1903. 

5.  Holmes.  An  outbreak  of  diphtheria  associated  with  a  similar 
disease  among  fowls  and  a  vesicular  eruption  on  the  udders  of  cows. 
Jour.  ofComp.  Path,  and  Tliera.,  Vol.  XVII  (1904),  P-  i- 

6.  Loeffler.  Untersuchungen  iiber  die  Bedeutung  der  Mikro- 
organisnien  fiir  die  Entstehung  der  Diphtherie  beim  Menschen,  beim 
Taube  und  beim  Kalbe.  Mitthiel.  a.  d.  Kaiserlichen  Gesundheitsamte, 
Bd.  II  (1884),  S.  421. 

7.  Loir  et  Ducloix.  Contributions  a  I'etude  de  la  diphterie 
aviare  en  Tunisie.     Ann.  de  /'  Inst.  Pasteur,  Vol.  VIII  (1894),  p.  559- 

8.  Mack.  The  etiology  and  morbid  anatomy  of  diphtheria  in 
chickens.     Am.  Vet.  Rev.,  Jan.,  1905. 

9.  Moore.  A  preliminary  investigation  of  diphtheria  in  fowls. 
Bulletin  No.  8.     U.  S.  Bureau  of  Animal  Industry,  1895. 

10.  Ransom.  Manson's  eye  worm  of  chickens.  Bulletin  No.  60. 
U.  S.  Bureau  of  Animal  Industry,  1904. 

11.  Salmon.     The  diseases  of  poultry ,  1899,  p.  216. 

12.  Ward.  Poultry  diseases  in  California.  Proceedings  of  the 
Amer.  Vet.  Med.  Asso.,  1904,  p.  164. 


INFLUENZA. 


Synonyms.  Epizootic  catarrhal  fever  ;  epizootic  catarrh  ; 
horse  distemper  ;  pink  eye  :  mountain  fever  ;  shipping  fever. 

i;  384.  Characterization.  Influenza  is  an  acute  infec- 
tious disease  characterized  by  a  rise  of  temperature  and  a 
catarrhal  condition  of  one  or  more  of  the  mucous  membranes, 
more  especially  of  the  head.  One  or  more  of  the  internal 
organs  may  become  affected.  It  usually  appears  in  epizootic 
form.     It  is  a  disease  of  honses,  although  asses  and  mules  are 


500  INFLUENZA 

susceptible  and  a  few  cases  are  reported  of  its  being  transmit- 
ted to  man  and  to  dogs.  It  appears  sometimes  in  sporadic 
form  and  often  in  epizootics. 

Influenza  is  a  generic  term  emploj-ed  to  designate  a  large 
variety  of  symptoms.  A  somewhat  careful  analysis  of  its 
manifestations  suggests  that  possibly  it  includes  a  number  of 
etiologically  distinct  diseases,  i.  e. ,  morbid  conditions  brought 
about  by  different  causative  factors.  The  term  has  long  been 
employed  to  designate  a  considerable  variety  of  equine  epizo- 
otics, the  independence  of  which  could  not  be  established. 
The  disease,  as  it  is  seen  in  the  horse,  suggests  further  that 
possibly  it  is  in  its  beginning  a  general  affection  because  of 
the  early  rise  of  temperature  and  that  later  in  its  course  it 
becomes,  to  a  limited  extent,  localized.  At  present  influenza 
is  restricted  to  groups  of  symptoms  and  lesions  in  the  horse 
that  are  not  verj^  unlike  those  of  la  grippe  in  man.  Its 
symptoms,  lesions  and  sequelae  warrant  such  a  view  at  least 
for  a  working  hypothesis.  As  it  is  not  usually  fatal,  little 
progress  seems  to  be  made  in  acquiring  knowledge  concerning 
the  nature  of  its  morbid  anatomy.  There  is  much  need  for 
careful  investigation  of  this  very  common  malady. 

^  385.  History.  According  to  the  writings  of  Falke, 
influenza  was  recognized  in  very  early  times.  There  is  evi- 
dence that  it  was  known  in  the  fourth  and  fifth  centuries.  It 
was  described  by  Low  in  1729  in  an  equine  epizootic  which 
had  spread  over  Southern  Europe.  It  is  also  stated  that  cases 
of  its  having  been  transmitted  to  man  had  occurred.  Gibson 
observed  it  in  1872  in  London  and  in  different  districts  of 
England.  It  raged  in  epizootics  in  1760,  1776  and. 1803.  The 
disease  was  widely  disseminated  during  the  last  century.  The 
more  important  epizootics  are  reported  in  the  years  from  18 13 
to  1815,  1825  to  1827,  1836  to  1840,  1846,  1851,  1853,  1862, 
1870,  1873,  1881  to  1883,  and  1890.  Anker,  who  described 
influenza  in  Switzerland  in  1826,  laid  stress  on  its  contagious 
nature  and  stated  that  in  his  opinion  "a  volatile  infectious 
matter  was  the  cause." 

Influenza  spread  as  an  epizootic  in   1872  to  1873  over  the 


ETIOLOGY 


-1-eater  part  of  the  United  States  where  it  received  the  name  of 
-pink  eve"  (French,  iTcvre  typhoide).  It  started  in  Canada 
and  extended  sonth  and  west,  reaching  into  British  Columbia 
to  the  north  and  Mexico  at  the  south.  The  last  great  epizo- 
otic raoed  in  Europe  from  1881  to  1883  during  which  time  11 
is  said  to  have  spread  over  nearly  the  whole  continent.  In  the 
Prussian  army,  3-434  horses  became  affected  in  1890  ;  2,497  m 
1891  ;  and  3.645  i"  ^^9^-  I"  Copenhagen,  3,000  horses  were 
affected  in  1890  and   1891. 

^  386  Geographical  distribution.  Influenza  seems  to 
be  known  in  nearlv  if  not  all  of  the  countries  of  Europe  and 
America  In  certain  sections  of  the  United  States  it  is  almost 
a  con.stant  affection.  This  is  especially  true  of  certain  cities, 
owing  to  the  constant  introduction  of  "green"  horses. 

§  387.  Etiology.  Influenza  seems  to  be  produced  by  a 
specific  infection  the  nature  of  which  has  not  yet  been  deter- 
mined A  number  of  bacteria  have  been  described  as  the 
probable  cause  but  thus  far  none  of  them  have  been  found  to 
be  sufficientlv  constant  to  warrant  their  acceptance  as  the 
etiological  factor.  It  spreads  rapidly  among  horses.  1  he 
virus  appears  to  lose  its  virulence  quickly  outside  of  the  animal 
body  but  within  the  body  it  seems  to  be  preserved  for  a  long 
time  According  to  the  observation  of  Jensen  and  Clark, 
stallions  which  have  had  the  disease  may  transmit  it  to  the 
mares  thev  serve  for  months  after  apparent  recovery.  Dieck- 
erhofi-  succeeded  in  transmitting  the  disea.se  to  healthy  animals 
bv  subcutaneous  and  intravenous  injections  of  the  blood  of  in- 
fected horses,  but  Friedberger  and  Arloing  failed  to  do  so. 
Horses  are  most  susceptible.  Sex,  breed,  stable  management 
and  feeding  appear  to  have  little  or  no  influence  on  their 
individual  su.sceptibility. 

Infection  usually  takes  place  from  horse  to  horse.  The 
virus  appears  to  be  carried  by  infected  human  beings,  litter, 
harnesses  and  thermometers.  In  many  cases  one  attack  con- 
fers immunity  but  a  second  infection  or  a  relapse  trequent  y 
occurs      Toward  the  end  of  an  epizootic  the  disease  is  usually 


502  INFLUENZA 

milder  in  form,  probably  due  to  a  gradual   attenuation   of  the 
virus. 

The  period  of  incubation  varies  from  two  to  seven  days. 
Siedamgrotzky  places  it  at  from  four  to  five  days  and  in  rare 
cases  from  12  to  24  hours.  In  some  cases  symptoms  have  not 
appeared  until  from  two  to  five  weeks  after  the  latest  known 
exposure. 

§  388.  Symptoms.  The  disease  appears  suddenly  and 
may  attain  its  highest  point  of  intensity  within  twenty-four 
hours.  The  organs  of  circulation,  nervous  centers,  digestive 
and  respiratory  mucous  membranes  and  conjunctiva  are 
especially  affected.  There  is  partial  or  entire  loss  of  appetite 
and  depression.  The  temperature  rises  suddenly  from  3  to 
4°  F.  or  even  more.  It  remains  high  with  but  slight  variations 
for  from  three  to  six  days  and  then  falls  rather  quickly,  often 
within  twenty-four  hours,  to  the  normal.  At  first  the  fre- 
quency of  the  pulse  is  but  little  increased  in  comparison  to  the 
elevation  of  the  temperature,  but  later  it  rises  to  from  60  to  70 
and  in  fatal  cases  from  80  to  100  or  more.  It  generally  con- 
tinues high  for  some  time  even  after  the  temperature  has 
fallen.  The  fever  is  characterized  by  unevenness  in  distribu- 
tion of  the  external  temperature  of  the  body.  The  early  rise 
of  temperature,  while  the  affected  horses  appear  to  be  healthy, 
is  of  much  diagnostic  value. 

Usually  the  nervous  depression  coexists  with  the  fever. 
The  animal  may  hold  its  head  down  and  appear  to  be  coma- 
tosed.  Extreme  muscular  debility  is  frequently  associated 
with  this  stupor.  Tremors  may  occur,  the  hind  legs  ma\^  give 
way  while  walking  and  paralysis  of  the  hind  quarters  appears 
in  a  few  cases. 

The  oral  mucous  membrane  is  greatly  congested,  hot,  dry 
or  covered  with  mucus.  There  is  sometimes  difficulty  in 
swallowing.  The  animal  frequently  yawns.  There  is  usually 
constipation  in  the  beginning  of  the  disease  which  may  be 
accompanied  with  colic.  The  feces  are  formed  into  small  hard 
balls  and  are   covered  with  masses  of  mucus.      Later  diarrhea 


SYMPTOMS  503 

with  considerable  teuesinus  usually  occurs  The  feces  are 
of  a  thin,  pulpy  and  even  fluid  consistence  and  sometimes 
have  a  fetid  odor.  At  the  beginning  of  the  attack  the  urine 
is  alkaline  but  it  becomes  acid  when  the  intestinal  lesions  are 
developed.  It  rarely  contains  albumin  but  desquamated  epi- 
thelial cells  of  the  bladder  are  often  present  in  large  quantity. 

A  severe  affection  of  the  eyes  is  quite  a  constant  charac- 
teristic symptom  of  influenza.  At  first  it  consists  chiefly  of  a 
catarrhal  and  later  of  a  phlegmonous  conjunctivitis  with  con- 
siderable swelling  of  the  eyelids,  which  may  be  followed  by 
keratitis  and  possibly  by  an  exudative  or  hemorragic  iritis. 
Usually  both  eyes  are  affected.  The  first  indications  are  the 
presence  of  tears,  intolerance  of  light,  intense  hyperemia  of 
the  conjunctiva  and  contraction  of  the  pupil.  The  eyelids 
swell,  are  hot,  painful  and  kept  more  or  less  continually 
closed.  A  gray,  muco-purulent  secretion  accumulates  be- 
tween the  eyeball  and  eyelids  and  the  eyeball  becomes  very 
sensitive  to  pressure.  The  cornea,  which  at  the  beginning  of 
the  keratitis  has  a  greasy  lustre,  first  becomes  iridescent,  but 
later  in  the  course  of  the  disease  it  may  be  opaque.  It  is  con- 
siderably injected  with  blood  at  its  edge  ;  the  iris  becomes 
swollen  and  yellowish  in  color.  Often  the.se  inflammatory 
changes  of  the  eye  disappear  in  a  strikingly  short  time. 

During  the  further  progress  of  the  disease,  swellings 
appear  on  the  extremities,  sheath,  epigastrium  and  lower  part 
of  the  chest.  It  may  be  concluded  that  these  swellings  are 
due  to  edema  caused  by  passive  congestion.  Less  frequently 
the  swellings  are  of  an  inflammatory  nature.  The  swelling  of 
the  extremities  causes  the  gait  to  be  stiff  and  un wieldly.  In- 
flammation of  the  sheaths  of  the  tendons  is  sometimes  ob.served. 

The  respiratory  mucosae  are  congested.  At  first  there  is 
a  -serous  and,  later  on,  a  muco-purulent  discharge  from  the 
nose,  slight  swelling  of  the  submaxillary  glands,  moderate 
acceleration  of  respiration  and  a  cough.  As  a  rule  the  animal 
becomes  emaciated  during  the  cour.se  of  the  disease.  Pregnant 
mares  may  abort. 

In  certain  cases  complications  may  ari.se,  such  as  cardiac 


504  INFLUENZA 

debility,  grave  cerebal  symptoms,  severe  gastro-intestinal 
inflammation,  laminitis  and  petechial  fever,  all  of  which  have 
been  described  as  accompanying  complications. 

The  duratioti  of  the  disease  is  from  six  to  ten  days,  although 
severe  cases  may  run  for  two  or  three  weeks  and  very  mild 
cases  may  recover  in  from  three  to  six  days. 

The  mortality  varies  at  different  times  and  in  different 
places.  The  average  appears  to  be  from  0.4  to  4  per  cent. 
Dieckerhoff  saw  a  loss  of  4  per  cent  among  1,700  horses; 
Aureggio,  one  of  3  per  cent  among  800  horses  ;  Friedberger, 
one  of  9  per  cent  ;  and  Siedamgrotzky,  one  of  10  per  cent.  It 
is  stated  that  in  1872,  in  Philadelphia,  7  per  cent  of  30,000 
infected  horses  died. 

§389.  Morbid  anatomy.  The  principal  tissue  changes 
of  influenza  are  met  with  in  the  organs  of  digestion.  The 
mucous  membrane  of  the  pyloric  portion  of  the  stomach  and  of 
the  intestines  is  hyperemic,  swollen  and  sprinkled  with  slight 
hemorrhages.  The  submucosa  is  yellowish  in  color  and  infil- 
trated with  a  gelatinous  substance  causing  the  membrane  to 
form  thick,  somewhat  translucent,  elevations  containing  a  fluid 
which  coagulates.  Peyer's  patches  are  enlarged,  especially 
those  in  the  neighborhood  of  the  ileo-cecal  valve.  The 
rnucous  membrane  of  the  mouth  and  sometimes  that  of  the 
pharynx  show  similar  changes. 

The  mucous  membrane  of  the  upper  air  passages  is 
hyperemic  and  swollen.  In  rare  cases,  the  mucosa  of  the 
larynx  is  inflamed,  also  the  subcutis  when  inflammatory  swell- 
ings appear  on  the  skin.  Schiitz  found  that  in  the  brain  and 
spinal  cord  the  arachnoid  spaces  are  filled  with  a  fluid  which 
is  generally  clear,  although  it  may  contain  leucocytes.  He 
reports  one  case  in  which  the  lateral  ventricles  contained  a 
large  quantity  (20  c.  c.)  of  fluid.  The  other  lesions  which 
may  be  found  depend  upon  the  extent  or  localization  of  the 
disease.  Usually  the  spleen  is  slightly  enlarged  ;  .small 
hemorrhages  in  the  intestines,  under  the  serous  membranes 
and  in  the  lungs,  eyes  and  brain  ;  gelatinous  infiltration  of  the 


DIFFERENTIAL  DIAflNOSIS  505 

renal  connective  tissue  and  mesentery  ;  swelling  of  the  lymph 
glands  ;  yellowish  serous  exudates  in  the  larger  cavities  of  the 
body  and  imperfect  coagulation  of  the  blood.  One  or  all  of 
these  changes  may  appear  in  a  single  animal. 

§  390.  Differential  diagnosis.  Influenza  must  be  dif- 
ferentiated from  strangles  and  contagious  pneumonia.  The 
differentiation  between  pleuro-pneumonia  and  influenza  is 
difficult  only  at  the  beginning,  when  merely  general  symp- 
toms, such  as  fever,  loss  of  appetite  and  weakness  are  present. 
It  should  be  mentioned  that  the  two  diseases  may  affect  the 
horse  simultaneously.  When  the  skin  is  greatly  swollen, 
influenza  may  resemble  petechial  fever,  from  which  it  can, 
however,  very  .soon  be  distinguished  by  the  absence  of 
petechiae,  by  the  mildness  of  its  course  and  its  greater  conta- 
giousness. In  case  of  strangles,  the  lesions  in  the  lymphatics 
may  serve  as  distinguishing  characters.  If  abscesses  are  in 
evidence  the  finding  of  the  streptococcus  of  strangles  would  be 
quite  conclusive.  It  would  be  positive  providing  streptococcus 
equi  could  readily  be  distinguished  from  the  pyogenic 
streptococci. 

With  these  diseases,  a  diagnosis,  save  in  the  more  typical 
forms,  is  difficult.  Without  a  definite,  recognizable,  etiologi- 
cal factor  or  other  exact  tests,  a  positive  diagnosis  in  doubtful 
cases  can  not  be  made. 

REFERENCES 

1.  LiGNiHRES.  The  etiology  of  equine  influenza  or  infectious 
pneumonia.    Jour,  of  Comp.  Path,  and  Thera.,    Vol.  XI   (189S),  p.  312. 

2.  M'Fadve.\n.  Influenza  of  the  horse — what  is  it?  Jour,  of 
Comp.  Path,  and  Thera.,  Vol.  II  (1889),  p.  105. 

3.  Marsden.  Influenza.  The  Vet.  Jour.  New  series.  Vol.  II 
(19C0),  p.  315.  (M.  describes  three  forms,  (i)  catarrhal  fever,  (2) 
bilious  fever,  (3)  epizootic  cellulitis. ) 

4.  Nelsox.  Influenza.  Bulletin  22.  State  Ai^ric.  Fxper.  Sta- 
tion, Washington.     1S96. 


506  DOG    DISTE.MPER 

DOG    DISTEMPER. 

Synonyms.  Dog  plague;  dog  disease;  bench  show  dis- 
ease; typhus  fever  in  the  dog;  typhoid  fever  iu  the  dog. 

§  391.  Characterization,  Distemper  is  an  infectious 
disease  appearing  in  sporadic  cases  or  in  epizootics.  It  is 
usually  determined  by  a  rise  of  temperature,  loss  of  appetite 
and  lassitude,  followed  by  a  catarrh  of  the  conjunctiva,  re- 
spiratory passages  and  digestive  tract.  Frequently  there  are 
serious  disturbances  of  the  nervous  system.  It  is  the  most 
important  canine  disease.  It  is  reported  that  cats,  wolves, 
foxes,  jackalls,  hyenas  and  monkeys  suffer  from  it. 

§  392.  History.  This  disease  of  dogs  was  known  in 
quite  early  times.  Its  history  shows  that  possibly  it  was  in- 
troduced into  Southern  Europe  from  Peru,  South  America, 
about  the  middle  of  the  eighteenth  century.  It  was  regarded 
as  being  closely  allied  to  a  number  of  diseases  of  the  human 
species  such  as  the  plague  and  typhus.  Trasbot  believed  it 
to  be  closely  allied  to,  if  not  identical  with,  small-pox. 

§  393.  Geographical  distribution.  Distemper  in  dogs 
is  a  widespread  disea.se.  It  is  exceedingly  common  in  the 
United  States  and  its  ravages  extend  throughout  America  and 
seem  to  be  no  less  in  Europe.  It  is  stated  that  there  is  no 
country  or  climate  in  which  the  dog  is  exempt  from  distemper. 

§  394.  Etiology.  The  specific  cause  of  distemper  has 
not  been  demonstrated.  A  large  number  and  variety  of  bac- 
teria have  been  thought  by  different  investigators  to  stand  in 
a  causal  relation  to  this  disease.  Schantyr  stated,  in  1891, 
that  canine  distemper  should  be  divided  into  three  different 
diseases  and  that  each  is  produced  by  a  distinct  species  of  bac- 
teria. More  recently  (1899)  Jess  has  isolated  a  bacillus  from 
the  catarrhal  secretions,  blood,  serous  exudates  and  organs. 
He  reports  having  reproduced  the  disease  in  dogs  with  pure 
cultures  of  this  organism.  The  writer  has  not  been  able  to 
find  this  bacillus  in  the  few  cases  which  he  has  examined,  but  a 


SVMI'TOM.S  507 

Streptococcus  has  often  appeared  in  pure  cultures  from  the 
various  organs.  Carre  has  shown  that  the  serous  discharge 
obtained  at  the  outset  of  the  disease  possesses  great  pathological 
power,  and  that  its  virulence  was  due  to  the  presence  of  an 
organism  suflficiently  small  to  pass  through  certain  filters. 
There  is  much  need  for  further  investigation  into  the  etiology 
of  this  malady.  That  it  is  produced  by  a  specific  cause  is  very 
clearly  indicated  by  the  reported  results  of  investigations  to 
the  effect  that  dogs  inoculated  with  the  nasal  discharge  of 
affected  animals  develop  the  disease. 

i^  395-  Symptoms.  The  symptoms  appear  after  a  period 
of  incubation  of  from  four  to  six,  possibly  eight  days.  They 
vary  to  such  a  degree  that  it  is  impossible  to  refer  to  all  of  the 
manifestations.  In  some  cases  the  symptoms  suggest  a  gen- 
eral disorder.  In  others  they  are  referable  to  certain  parts  or 
organs  such  as  the  mucosa  of  the  digestive  and  respiratory 
tracts,  the  brain  or  integument.  As  a  rule  several  organs  are 
implicated. 

The  initial  symptoms  such  as  depression,  roughened  con- 
dition of  the  coat,  lo.ss  of  appetite  and  elevation  of  temperature 
are  suggestive  of  a  general  disturbance. 

In  a  large  majority  of  cases,  conjunctivitis  is  the  primary 
ocular  symptom.  Tears  flow  from  the  eyes  and  photophobia 
is  present.  The  mucous  membrane  of  the  eyelids  becomes 
conjested  and  a  purulent  exudate  may  appear.  The  exuded 
matter  consists  of  pa.sty  mucous  or  dirty  yellowish  pus.  This 
exudate  collects  under  the  lower  eyelids,  chiefly  at  the  inner 
canthus  of  the  eye  and  soils  the  edges  of  the  eyelids,  upon 
which  it  frequently  dries  and  causes  the  lids  to  adhere,  espec- 
ially during  the  night.  Ulcers  form  on  the  cornea  in  conse- 
quence of  the  action  of  the  accumulated  and  decomposing  pus 
and  the  patient  wiping  and  rubbing  the  eyes  with  its  paws. 
The  epithelium  of  the  cornea  sometimes  suffers  more  or  less 
from  shallow  flat  lesions  which  give  the  surface  of  the  cornea  a 
rough  and  uneven  appearance.  Frequently  smaller  and  deeper 
ulcers  form  especially  toward  the  center  of  the  cornea. 


508  DOG    DISTEMPER 

In  Other  cases,  there  is  a  diffuse,  parenchymatous  keratitis 
which  renders  the  cornea,  to  a  considerable  extent,  opaque  and 
gives  it  the  appearance  of  ground  glass.  These  extensive 
opacities  sometimes  develop  in  a  comparativeh-  short  time. 
This  affection  of  the  cornea,  the  so-called  "distemper  of  the 
eyes,"  is  frequently  the  only  evidence  of  distemper  with  the 
exception  of  the  high  temperature. 

There  may  be  vomiting,  well  marked  congestion  and  dry- 
ness of  the  oral  mucosa.  There  is  usually  constipation  at 
first,  but  later  a  diarrhea  in  which  the  feces,  as  a  rule,  are 
very  fetid,  often  slimy  and  frothy.  Hemorrhagic  intestinal 
catarrh  sometimes  exists.  The  urine  frequently  contains 
albumin  and  bile  pigment,  especially  when  the  patient  is  weak 
or  in  an  advanced  stage  of  the  disease. 

The  nasal  discharge  is  serous  at  first,  mucous  or  purulent 
later  on.  It  is  followed  by  sneezing,  panting  and  a  nasal  pru- 
ritis,  which  causes  the  animal  to  rub  its  nose  with  its  paws. 
The  purulent  discharge  from  both  nostrils  may  be  very  copious. 
It  is  sometimes  mixed  with  streaks  of  blood,  and  varies  in 
color  from  a  dirty  yellow  to  a  dirty  green.  Later,  it  may  be- 
come fetid  and  even  watery.  Ulcers  may  appear  on  the  nasal 
mucosa. 

Laryngeal  catarrh  usually  accompanies  the  nasal  catarrh 
and  manifests  itself  by  a  cough,  which  comes  on  in  paroxysms 
and  which  is  at  first  hoarse  and  dry,  but  later  moist  and 
accompanied  by  a  discharge  of  phlegm.  The  cough  excites 
vomiting.  The  catarrh  spreads  from  the  larynx  to  the  trachea 
and  bronchi.  The  resulting  bronchitis  is  followed  by  an  in- 
creased rate  of  breathing  and  manifests  itself  b}'  a  cough  and 
hoarse,  sharp,  vesicular,  respiratory  murmurs.  Frequentlj- 
there  is  a  catarrh  of  the  mucous  membrane  of  the  smaller 
bronchi.  There  may  be  difficulty  in  breathing  and  a  feeble 
cough  which  the  patients  try  to  suppress.  The  cough  may  be 
excited  by  percussion  of  the  thoracic  walls,  by  the  animals 
getting  up  and  by  their  being  taken  out  of  their  kennels. 
Young  and  weak  animals  that  cannot  remove  the  accumulated 
phlegm  from  the   bronchi  by  coughing  become   affected   with 


SYMPTOMS  509 

catarrhal  pneumonia.     The  pneumonia  can  be   recognized   by 
the  elevation  of  the  temperature. 

Distemper  often  begins,  especially  in  anemic  animals,  with 
great  depression  and  dullness.  Strong  animals,  however,  more 
usually  exhibit  symptoms  of  acute  hyperemia  of  the  brain, 
such  as  excitement,  restlessness,  yelping  and  even  attacks  of 
fury,  which  give  way  later  on  to  manifestations  of  cerebral 
pressure.  Spasms  frequently  occur  either  generally  or  con- 
fined to  particular  limbs  which  swing  backward  and  forward 
as  if  affected  by  chorea.  The  animal  may  fall  down  as  if  suf- 
fering from  epilepsy,  bark,  become  unconscious  and  exhibit 
.spasms  of  the  muscles  generally.  The  sphincters  of  the  anus 
and  bladder  become  relaxed  and  consequently  feces  and  urine 
are  involuntarily  passed.  There  is  a  gradual  return  of  con- 
sciousness which  in  a  short  time  is  complete  and  the  dog 
manages  to  get  up,  although  he  is  very  weak.  Such  an  epi- 
leptiform attack  may  pass  directly  into  long  continued  coma. 

Paralysis  may  follow  the  convulsions  or  it  may  come  on 
simultaneously  with  them.  It  seldom  occurs  at  the  beginning 
of  the  disease.  It  may  be  confined  to  certain  groups  of  muscles, 
as  those  of  a  limb,  the  whole  of  the  hind  quarters  or  even 
the  entire  body  in  the  form  of  paresis,  especially  of  the  motor 
nerves,  combined  with  excessive  muscular  weakness.  The 
sick  dog  staggers  and  his  hind  quarters  sway  from  side  to  side 
or  he  becomes  incapable  of  supporting  him.self  on  his  hind 
legs.  Frequently  he  knuckles  on  all  four  legs  and  in  severe 
cases  is  unable  to  stand.  Permanent  paresis  of  the  hind  quar- 
ters with  paralysis  of  the  bladder  and  rectum  is  a  frequent 
result  of  distemper.  In  some  cases  there  may  be  paralysis  of 
the  muscles  of  the  tongue. 

A  characteristic  pustular  exanthema  is  frequently  observed 
on  the  inner  surface  of  the  thighs  and  abdomen  and  in  abor- 
tive cases  it  may  be  the  only  symptom  of  distemper.  It  first 
appears  in  the  form  of  minute  red  spots,  which  after  twenty- 
four  hours  develop  into  miliary  nodules  that  are  surrounded  by 
a  red  ring.  These  nodules  change  into  vesicles  and  pustules 
which  may  become  as  large  as  a  pea  or  bean.     They   dry    into 


5IO  DOG    DISTEMPER 

a  5'ellowish  brown  crust  or  burst,  leaving  a  raw  surface.  Heal- 
ing takes  place  with  desquamation  of  the  epidermis  after 
about  eight  days,  leaving  pigmented,  pale  reddish  areas  which 
persist  for  some  time.  Generally,  there  are  only  a  few  pus- 
tules present.  The  exanthema  may  spread  in  the  form  of  a 
scabby  eczema  over  the  whole  body,  to  the  membrane  of  the 
external  auditory  meatus  and  less  frequently  to  the  mucous 
membrane  of  the  mouth  and  eyes.  This  eruption,  contrary  to 
that  of  sarcoptic  mange,  is  accompanied  by  only  slight  pruritis. 
Intense  catarrh  of  the  prepuce  may  appear  simultaneouslj- 
with  the  skin  eruption. 

The  temperature,  which  is  usually  very  irregular,  is 
higher  during  the  initial  stage  than  when  local  manifestations 
appear.  It  often  falls  with  remarkable  rapidity  below  normal 
towards  the  approach  of  death.  If  the  disease  runs  a  pro- 
tracted course,  the  patient  becomes  emaciated  and  the  hair 
loses  its  lustre,  the  body  exhalations  have  a  very  fetid  odor, 
the  eyes  are  sunken,  the  mucous  membranes  become  pale  and 
the  patient  grows  weaker,  staggers  when  walking  or  lies  in  a 
state  of  coma. 

In  abortive  cases  recovery  may  take  place  in  eight  or  ten 
days,  although  the  disease  usually  lasts  three  or  four  weeks. 
With  severe  complications,  especially  those  of  the  nervous 
system,  distemper  assumes  a  protracted  course  and  is  frequently 
followed  by  sequelae,  such  as  paralysis  or  convulsions  at 
longer  or  shorter  intervals,  which  may  persist  for  months  and 
even  longer.  The  average  mortalitj^  appears  to  be  from  50  to 
60  per  cent. 

§  396,  Morbid  anatomy.  The  anatomical  changes  in 
the  respirator}--  system  are  those  of  rhinitis,  laryngitis,  bron- 
chitis and  catarrhal  pneumonia.  The  nasal  mucous  membrane 
is  either  very  pale  or  greatly  congested,  swollen  and  covered 
with  a  thick,  purulent,  grayish  green  or  dull  reddish  inflam- 
matory exudate  which  is  mixed  with  coagulated  blood  and 
collects  chiefly  between  the  lamellae  of  the  turbinated  bones 
and  in   the   frontal   sinuses.     Hemorrhagic  ulcers   are   some- 


MORHID    ANATOMY  5II 

times  present.  The  mucous  membrane  of  the  larynx  and 
bronchi  is  hyperemic,  swollen,  often  infiltrated  with  hemor- 
rhages and  covered  with  pus.  Sometimes  catarrhal  ulcers 
appear.  The  large  bronchial  tubes  often  fail  to  exhibit 
changes  which  might  have  been  expected  from  the  symptoms. 
The  smaller  bronchi  are  on  the  other  hand  frequently  filled 
with  a  dirty  gray  and  even  bloody,  viscid  pus.  There  are 
areas  of  congestion  on  the  surface  of  the  lungs,  some  parts  of 
which  may  contain  but  little  air.  There  may  be  areas  of  col- 
lapse or  those  abnormally  filled  with  air.  The  inflammatory 
foci  of  the  lungs  are  usually  consolidated.  In  very  young 
animals  there  may  be  a  fibrinous  exudate  which  is  very  soft 
and  which  readily  liquefies.  The  hepatization  frequently 
involves  an  entire  lobe.  The  hepatized  parts  are  frequently 
studded  with  small  suppurating  foci,  or  are  difFu.sely  infiltrated 
with  pus.  The  pleura  over  the  affected  parts  is  often  inflamed. 
The  bronchial  glands  are  swollen  or  infiltrated  with  a  serous 
fluid  or  with  pus. 

In  the  digestive  system,  the  mucous  membrane  of  the 
stomach  and  intestines,  especially  that  of  the  small  intestine, 
is  hyperemic  and  swollen.  It  may  be  covered  with  a  tough 
mucus  and  is  often  sprinkled  with  hemorrhages.  In  other  cases 
it  is  very  pale,  swollen  and  easily  torn.  Frequently  the  con- 
tents of  the  intestine  are  blood  stained  and  the  mesenteric 
glands  enlarged  and  edematous. 

The  brain  is  anemic  and  often  there  is  a  .serous  effusion 
into  the  lateral  ventricles  and  subarachnoid  spaces.  In  a  few 
cases  there  are  signs  of  a  purely  venous,  cerebral  hyperemia, 
as  for  instance,  great  congestion  of  all  the  sinuses,  venous 
plexuses  and  vessels  of  the  pia  and  the  appearance  on  the  cut 
surfaces  of  the  brain  of  numerous  blood  points  which  can  easily 
be  wiped  off.  Kolesnikoff  found  microscopically  the  brain 
substance,  especially  the  walls  of  the  vessels,  infiltrated  with 
leucocytes.  Krajewski  noticed  dilation  of  the  vessels,  cellular 
infiltration  of  their  walls,  filling  of  the  perivascular  spaces 
with  lymphoid  cells  and  migration  of  lymphoid  cells  into  the 
stroma  of  the  brain  and  into  tlie  protoplasm  of  the   ganglionic 


512  DOG    DISTEMPER 

cells.  The  changes  in  the  spinal  cord,  which  are  not  well 
marked,  consist  chiefly  of  anemia  and  slight  edema,  especially 
in  the  lumbar  region.  Maznlewitsch  states  that  in  acute 
paralysis  there  are  changes  in  the  walls  of  vessels,  with  an 
exudate  along  the  vessels  and  in  the  interstitial  tissue  of  the 
gray  matter  of  the  spinal  cord.  In  chronic  distemper,  there  is 
a  localized  interstitial  myelitis  with  partial  atrophy  of  the 
cord.  Hadden  found  groups  of  emigrated  blood  corpuscles  in 
it.  In  severe  cases,  according  to  Trasbot,  the  spinal  cord  and 
its  membranes  are  often  considerably  injected  with  a  sero- 
fibrinous exudate  in  and  under  the  arachnoid  and  even  into 
the  substance  of  the  spinal  cord. 

Among  the  other  changes  which  have  been  described  we 
may  mention  decrease  in  the  total  quantity  of  the  blood  of  the 
body,  combined  with  a  certain  degree  of  hydremia.  There 
may  be  fatty  degeneration  of  the  liver  and  kidneys.  The 
muscular  tissue  of  the  heart  is  discolored  in  consequence  of 
cloudy  swelling  and  fatty  degeneration  of  the  fibers.  The 
lymph  glands  may  be  edematous. 

^  397.  Differential  diagnosis.  Distemper  is  to  be  dif- 
ferentiated from  : 

1.  A  simple  catarrh,  such  as  that  of  the  eyes,  nose, 
lungs,  stomach  or  intestines.  The  differentiation  is  often  diffi- 
cult at  first,  as  distemper  frequently  manifests  itself  in  a  single 
mucous  membrane  or  in  one  organ.  In  general  the  diagnosis 
is  obtained  from  the  epizootic  nature  of  the  disease,  age  of 
the  patient,  high  temperature,  simultaneous  implications  of 
several  organs  and  the  unfavorable  course  of  the  malady.  The 
finding  of  the  pustules  of  dog  distemper  is  of  much  diagnostic 
value. 

2.  Rabies.  The  symptoms  of  cerebral  irritation  which 
occur  at  the  beginning  of  the  disease  may  give  rise  to  the 
suspicion  of  rabies.  The  characteristic  aggressive  behavior  of 
animals  suffering  from  rabies  is,  however,  absent  in  cases  of 
distemper.  The  further  course  of  the  disease  soon  enables  a 
diagnosis  to  be  made. 


PRKVKNTION  513 

3.  The  eruption  of  distemper  if  widely  distributed  over 
the  body  may  resemble  that  of  mange.  The  mild  character  of 
the  pruritis,  the  presence  of  pustules  on  the  hypogastrium  and 
inner  surface  of  the  thighs,  the  rapid  spreading  of  the  exan- 
thema over  the  whole  body  and  the  development  of  other 
symptoms  of  distemper  and  those  of  mange,  however,  often  oc- 
cur simultaneously  in  the  same  animal,  in  which  cases  certain 
precautions  are  necessary  in  making  the  correct  diagnosis. 

4.  Epilepsy.  The  epileptiform  attacks  in  distemper  are 
distinguished  from  true  epilepsy,  essentially  by  their  being  less 
acute. 

5.  It  must  also  be  differentiated  from  simple  coryza, 
bronchitis,  chorea  and  paralysis. 

Until  the  specific  cause  is  found  and  can  be  availed  of  in 
making  the  diagnosis,  much  doubt  will  necessarily  exist  re- 
specting the  nature  of  the  disease  where  many  of  the  symptoms 
and  lesions  are  atypical.  It  may  be  found  on  further  investi- 
gation and  the  discovery  of  the  etiological  factors  that  the 
symptom-complex  of  distemper  may  be  differentiated  into  two 
or  more  distinct  affections. 

ij  398.      Prevention.     The  lack  of  knowledge  concerning 

the  specific  cause  has  rendered  it  impossible   thus  far  to  close 

all  channels  of  infection,  but  its  spreading  can  be  checked  to  a 

considerable  degree  by  isolation  and  the  use  of  disinfectants. 

It  has  been  stated  that  the  inoculation    with    the   virus    from 

very  mild  cases,  which  produces  a  mild  attack,  will  immunize 

an  animal  for  several  years.     This  method  is  as  a  rule  not  to 

be  recommended. 

rkfkrp;ncks. 

1.  C.-VRRK.  Sur  la  "Maladie  des  chiens."  Rtil.  de  la  Soc.  Ccutr. 
lie  Med  VH.,  Vol.  I.IX  (1905),  p.  335- 

2.  Hertwig.     Krankheiten  der  Huiide.     1S81.     S.  48. 

3.  jKss.  Der  Bacillus  der  Hundestaupe  (Febris  catarrhalis  epizo- 
otica  Canum.)     Cent.  f.  Bak.  u.  Parasiteuk.,  Bd.  XXV  (1S99),  vS.  541. 

4.  Laossom.  I'eber  Geschichte  und  KontagiositHt  der  Staupe. 
Dorpat.     1892. 

5.  NiCKOi.DS.     Dog  distemjier.     Am.    I'ei.  Reviezc,  1900.     j).  180. 


514  CEREBRO-SPIXAL    MENINGITIS 

CEREBRO-SPINAL  MENINGITIS  IN  HORSES. 

SjJionvfus.  Staggers  ;  craz\-  disease  :  forage  poisoning  ; 
acute  epizootic  leucoencephalitis. 

^  399.  Characterization.  This  is  a  disease  that  seems 
to  be  infectious  in  its  nature,  exhibiting  s\-mptonis  referable  to 
a  disturbance  in  the  central  nervous  system.  It  is  called 
epizootic  cerebro-spinal  meningitis  because  it  often  attacks  a 
number  of  animals  in  the  same  locality.  It  often  occurs  in 
sporadic  ca.ses.  Although  the  literature  contains  numerous 
accounts  of  its  seemingly  contagious  nature,  an  analysis  of  the 
facts  fails  to  bring  forth  conclusive  evidence  that  it  is  ever 
transmitted  directly  from  one  horse  to  another.  In  nearly  if 
not  all  outbreaks,  the  animals  affected  have  been  subjected  to 
like  conditions  of  life.  This  disease  is,  at  the  present  time, 
peculiar  in  that  its  cause  is  not  known,  that  obvious  tissue 
changes  are  usually  absent,  and  that  it  has  a  very  high 
mortality. 

J^  400.  Etiology.  The  cause  has  been  attributed  to  a 
great  variety  of  conditions,  such  as  fermented  food,  forage 
laden  with  fungi  or  toxic  moulds,  various  unsanitary  con- 
ditions and  possibly  other  ill-defined  agencies.  It  seems  to  be 
true  that  in  most  outbreaks  all  of  the  animals  that  suffer  have 
had  at  least  some  one  thing  in  common  either  in  surroundings, 
food  or  management.  The  bacteriological  and  other  examina- 
tions which  have  been  made  to  determine  the  cause  have  not 
resulted  in  finding  a  specific  agent.  Micrococci  and  various 
bacilli  have  been  found  associated  with  the  disease.  The 
writer  has  had  an  opportunity  of  making  a  careful  examina- 
tion of  animals  in  two  outbreaks.  In  one  of  them  all  inocu- 
lated media  and  histological  examinations  gave  negative 
results,  in  the  other  pure  cultures  of  a  colon  bacillus  were  ob- 
tained from  the  brain.  No  specific  organism,  therefore,  is 
charged  with  its  production.  Xo  virus  has  been  isolated  that 
is  capable  of  producing  it.  The  nature  of  the  affection  sug- 
gests a  poison  rather  than  a  specific  virus. 


SYMPTOMS  5'5 

j^  401.  Symptoms.  The  mildest  attacks  are  manifested 
by  paresis  or  loss  of  perfect  control  over  the  limbs,  loss  of 
power  over  the  tail,  impairment  of  appetite  and  some  difficulty 
in  swallowing,  together  with  areas  of  hyperemia  and  reddish- 
brown  discoloration  of  the  orbital  and  nasal  mucosae.  In 
other  cases  paralysis  of  one  or  more  limbs  may  supervene  but 
without  marked  fever  or  coma. 

The  more  severe  forms  are  ushered  in  by  violent  tremb- 
ling, or  by  stupor,  apathy  and  extreme  muscular  weakness  or 
actual  paralysis.      In  such  cases  the    animal    may    stagger   or 
fall.     The  inability  to  swallow  is  often  a  marked  symptom,  the 
saliva    falling    in    strings    from    the    lips.       Another  common 
phenomenon    is    the    rigid   contraction  of  the    muscles  of  the 
neck,  back  and  loins,  the  parts  becoming  tender  to  the  touch 
and  a  more  or  less  prominent  opisthotonos  setting  in.    Twitch- 
ing of  the  muscles  of  the  shoulders  and  flanks  may  be  noticed. 
Trismus   is  sometimes   seen.     The  breathing  is  usually  rapid 
and  catchy  and  the  temperature  ranges  from   104°   to   106°  F. 
The  pulse  may  be  accelerated  and  hard,  soft  and  weak,  or  al- 
ternating.      The    eyes   are  usually   violently  congested,  of  a 
brownish    or    yellowish-red    color,  and    the    eyeballs   may    be 
turned  to  one  side.     Paroxysms  of  delirium  may  set  in   when 
the  animal  will  push  against  the   wall  or  perform   any  of  the 
disorderly  movements  following  meningo-encephalitis.    Sooner 
or  later  coma  and  paralysis  supervene  and  death  occurs  in  from 
five  to  forty-eight  hours.     In  the  most  acute  cases  the  animal 
falls  and  dies  in  convulsions.     On  an  average  the  disease  lasts 
from   eight   to  fourteen  days.      In   the  more  favorable  cases, 
improvement  may   begin  on   the   third  or    fourth    day.     One 
attack  does  not  protect  the  animal  against  a  subsequent  one. 

jj  402.  Morbid  anatomy.  Most  writers  report  lesions  of 
leptomeningitis,  hyperemia  of  the  brain  and  .spinal  cord,  with 
extensive  effusion  into  the  ventricles  and  subarachnoid  spaces. 
Petechia;  and  parenchymatous  degeneration  of  the  solid  organs 
of  the  body  are  also  mentioned.  In  the  cases  examined  by 
the  writer  tiiere  has  been  an  absence  of  lesions  in  the  nervous 


5l6  CEREBRO-SPINAL     MENINGITIS 

system  and  other  organs  that  could  be  detected  by  a  gross 
examination.  In  one  case  the  brain,  spinal  cord,  and  organs 
were  studied  histologically  with  like  results. 

MacCallum  and  Buckley  have  found  in  the  brains  of 
horses  dying  of  this  disease  areas  of  softening  "  in  the  frontal 
region  on  each  side,  anterior  to  the  motor  region  of  the 
cortex."  This  lesion  was  practically  confined  to  the  white 
matter  immediately  under  the  cortex.  In  the  affected  areas 
there  was  "complete  destruction  of  the  brain  substance,  in 
which  the  anatomical  structures  are  disintegrated  and  largely 
replaced  by  a  colloid-like  material  ".  The  neighboring  blood 
vessels  were  acutely  inflamed,  with  exudation  of  leucocytes 
and  passage  of  red  corpuscles  into  the  peri-vascular  lymph 
sheath  and  adjacent  tissue.  In  a  later  epizootic  they  failed  to 
find  the  brain  lesion  but  did  detect  the  vascular  changes. 

McCarthy  and  Ravenel  in  a  study  of  fifteen  animals  found 
certain  lesions  in  the  upper  gastrointestinal  tract  and  in  the 
central  nervous  system.  These  were'(i)  in  the  intervertebral 
and  Gasserian  ganglia  where  a  peri-capsular,  small  round  cell 
accumulation  was  present.  The  cells  were  all  of  the  same 
type,  the  nucleus  and  protoplasm  being  about  the  size  of  a  red 
corpuscle.  There  was  no  evidence  that  these  cells  were  the 
result  of  proliferation  of  the  original  layer  of  capsular  cells. 
(2)  Cortical  lesion.  These  consisted  of  congestion  of  the 
cerebellar  and  cerebral  cortex.  There  were  also  capillary 
hemorrhages.  The  meninges  were  normal.  (  t,)  Changes  in 
the  choroid  plexus.  In  three  cases  the  choroid  plexus  was 
changed  into  a  triangular,  tumor-like  mass,  of  a  yellowish  red 
color  and  of  a  firm  consistency.  .  The  increase  in  size  was 
found  to  be  due  to  a  proliferation  of  the  elastic  tissue  sur- 
rounding the  vessels.  (4)  Changes  in  the  peripheral  nerves. 
There  was  a  distinct  degeneration  of  the  nerves  supplying  the 
larynx  and  neck.  This  was  present  in  the  nerve  up  to  the 
ganglion,  but  was  not  found  in  the  posterior  roots.  Other 
slight  changes  were  detected. 

These  authors  conclude  that  this  disease  is  not  a  true 
meningitis,  but  that  the  evidence  goes  to  show  that  it  is  caused 


CORNSTALK    DISKASE    IN    CATTLE  517 

by  some  poisonous  substance  contained  in  the  forage.  They 
propose  the  name  "forage  poisoning"  tor  "cerebrospinal 
meningitis"  and  leucoencephalitis  suggested  by  MacCallum 
and  Buckley.  It  is  highly  probable  that  up  to  the  present 
time,  cases  of  uncomplicated  meningitis  and  possibly  cerebritis 
have  been  confused  with  the  disease  in  question.  The  entire 
subject  must  await  the  results  of  further  investigation. 

§  403.  Differential  diagnosis.  This  disease  is  to  be 
differentiated  from  other  forms  of  cerebral  affection  and  rabies. 
The  differentiation  can  be  made  from  the  clinical  history  of 
the  case,  and  from  the  character  of  the  lesion  in  the  interver- 
tebral ganglia  and  if  necessary  by  the  results  of  animal 
inoculation. 

RKFERKNCES. 

1.  Favillk.  So-called  spinal  meningitis.  Am.  Vet.  Revieio, 
Vol.  XVII,  p.  9. 

2.  Hickman.  Epizoc'itic  cerebro-spiual  meningitis  of  horses. 
Tzcoity-tlnrd  annual  report,  Jlureau  0/  Animal  Industry,  1906. 

3.  Martin.     Cerebro-spinal  meningitis.    Ibid.    Vol.  XXI,  p.  289. 

4.  McCallum  .and  Buckley.  Acute  epizootic  Leucoencephalitis 
in  horses.     Bulletin  No.  So,  3Id.  Agric,  Exp.  Station,  1902. 

5.  McCarthy  and  Ravenel.  A  pathology  for  forage  poisoning, 
or  the  so-called  epizootic  cerebro-spinal  meningitis  of  horses.  The 
Journal  of  Medical  Research,  Vol.  X  (1903),  p.  243. 

6.  SiEDAMGRoTZKY  AND  ScHLEGKL.  Kpizootic  cerebro-spinal 
meningitis  in  the  horse.  Archiv  fi'ir  zviss.  u.  prakt.  Thicrheilk.  Bd. 
XXII.      (.lbstract),y(7«;-.  Com.  Path,  and  Thera.,  Vol.  IX,  p.  233. 


CORNSTALK   DISE.\SE  IX  CATTLE. 

^  404.  Characterization.  The  name  "cornstalk  disease" 
has  been  given  to  a  somewhat  mysterious  affection  from  which 
cattle  sometimes  suffer  while  feeding  in  cornstalk  fields  late  in 
the  fall  and  early  winter.  The  meaning  generally  accepted 
and  intended  to  be  conveyed  by  this  term  is,  that  an  animal  or 
a  number  of  animals,  usually  cattle,  have  died  suddenly  after 
feeding  in   a   corn.stalk  field   from   four  to  ten  da\  s.      From  a 


5l8  CORNSTALK    DISEASE    IN    CATTLE 

pathological  point  of  view,  therefore,  the  term  is  meaningless, 
but  it  has  served  admirably  as  a  general  term  to  designate  cer- 
tain fatalities  occurring  under  a  given  condition,  which  are 
not  easily  explained. 

This  disease  is  very  insidious,  frequently  causing  the 
death  of  animals  before  its  presence  is  suspected.  Cattle  that 
act  perfectly  well  at  night  are  dead  on  the  following  morning. 
Usually  all  the  animals  in  the  herd  that  die  of  this  affection 
perish  in  a  single  night  or  at  the  longest  within  a  few  days 
after  the  first  death  occurs.  It  is  generally  believed  to  be  in- 
variably fatal  and  its  symptomatology  has  not  been  fully 
determined. 

§  405.  History.  This  affection  of  cattle  has  been  known 
to  exist  for  many  years.  The  time  and  place  of  its  origin, 
however,  are  not  known,  but  it  seems  to  be  peculiar  to  the 
United  States  and  to  have  first  appeared  west  of  the  Alle- 
gheny Mountains.  We  are  told  of  its  occurrence  in  the  Mis- 
sissippi Valley  forty  or  more  years  ago.  It  made  extensive 
ravages  in  1864-65  and  again  in  1868.  PVom  an  historical 
standpoint,  no  positive  statements  can  be  made  concerning  it 
prior  to  1868,  when  the  first  recorded  investigations  into  its 
nature  and  cause  were  made.  After  that  time  the  disease 
seems  to  have  escaped  the  attention  of  investigators  until  1889, 
when  Billings,  of  the  Agricultural  Experiment  Station  of 
Nebraska,  published  the  results  of  his  investigations. 

In  1868,  Gamgee  was  employed  by  the  United  States 
Department  of  Agriculture  to  investigate  this  disease.  The 
"smut  theory"  of  its  etiology  appears  to  have  been  the  pre- 
vailing one  at  that  time  and  consequently  Gamgee's  report 
deals  almost  exclusiveh*  with  the  effect  of  improperly  prepared 
food,  smuts  and  the  like.  Corn  smut  was  unusually  abundant 
in  1868  and  he  carried  out  experiments  to  test  its  etiological 
value  with  the  conclusion  ' '  that  smut  is  not  a  very  active 
poison  in  combination  with  wholesome  food.'' 

In  1889,  Billings  described  the  cornstalk  disease  as  an 
"acute    extraorganismal   septicemia,    due   to    micro-organisms 


HISTOKV  519 

belonging  to  the  class  of  ovoid-belted  germs,  to  which  vari£ty 
of  disease  also  belongs  the  swine  plague,  southern  cattle 
plague.  Wildescuche,  hog  cholera,  and  yellow  fever  in  man.  " 
BVom  the  organs  of  cattle  dead  from  the  disease  he  reported  to 
have  invariably  isolated  a  bacillus  which  he  affirms  to  be  its 
cause.  He  identified  the  bacillus  which  he  found  in  the 
animal  tissues  with  the  one  described  by  Burrill  as  the  cause 
of  a  disease  in  cornstalks.  In  1893,  Dr.  Theobald  Smith  iden- 
tified the  bacillus  described  by  Professor  Burrill  as  Bacillus 
cloaca-. 

Billings  also  found  pneumonia  to  l)e  one  of  the  lesions 
characteristic  of  this  affection  and  in  a  subsequent  bulletin  he 
places  great  importance  upon  this  lesion,  although  he  adds 
very  few  additional  observations  to  sustain  the  claim. 

In  1890,  a  few  animals  from  a  shipload  of  American  cattle 
landed  at  La  \'illette,  France,  died  of  pneumonia.  They  were 
examined  very  carefully  by  Nocard  and  other  French  veterin- 
arians. From  the  diseased  lung  Nocard  obtained  a  micro- 
organism which  corresponded  very  closely  to  the  description  of 
the  bacillus  of  the  corn.stalk  disease  of  cattle  described  by 
Billings  in  America.  The  publication  of  this  fact  gave  rise  to 
a  temporary  supposition  that  this  American  cornstalk  disease 
might  be  a  menace  to  the  cattle  of  Europe  and  consequently 
initial  steps  were  taken  to  require  American  cattle  to  be  (quar- 
antined against  it.  The  fact  was  subsequently  determined 
that  the  bacillus  isolated  by  Nocard  belonged  to  the  septicemia 
hemorrhagica  group  of  bacteria  which  is  usually  found  to  be 
associated  with  a  form  of  bovine  pneumonia  occasionally  met 
with  in  America,  but  not  known  to  be  contagious,  and  the 
matter  was  dropped. 

A  single  experiment  was  made  at  Champaign.  Ill  ,  in 
1889.  in  which  the  etiological  importance  of  corn  smut  was 
tested  with  negative  results.  A  bacteriological  examination 
of  the  organs  from  an  animal  that  died  in  a  cornstalk  field, 
supposedly  of  this  disease,  was  made  with  negative  results  by 
Professor  Burrill  in  1889. 

In    1892,    Moore  investigated  this  disease  and  his  report 


520  CORNSTALK    DISEASE    IN    CATTLE 

furnishes  the  information  here  given  concerning  the  symptoms 
and  morbid  anatomy  of  this  affection. 

§  406.  Geographical  distribution.  Geographically, 
this  affection  is  restricted  very  largely  to  those  sections  of  the 
United  States  where  the  farmers  harvest  their  corn  by  picking 
the  ears  from  the  standing  stalks,  after  which  cattle  are  turned 
into  the  cornstalk  fields.  At  present,  therefore,  it  is  limited 
in  its  distribution  to  the  middle  and  northern  portions  of  the 
Mississippi  Valley.  It  is  believed  that  there  are  exceptions  to 
this  and  that  infrequently  cattle  die  from  its  effects  in  the 
eastern  part  of  the  country. 

vj  407.  Etiology.  The  definite  cause  of  this  disease  has 
not  been  determined.  It  has  been  shown,  however,  that  the 
former  theories  respecting  salt,  water  and  the  bacillus  of  the 
Burrill  disease  of  cornstalks  are  not  substantiated.  The 
hypothesis  that  the  cause  rests  in  the  cornstalks  themselves 
seems  to  be  the  most  tenable.  It  is  well  known  that  cattle 
rarely  if  ever  die  from  eating  cornstalks  in  moderate  quanti- 
ties. However,  the  results  of  such  investigations  as  have  been 
made  point  as  the  cause  to  an  intoxication  from  an  excessive 
quantity  of  one  or  more  elements  existing  in  the  cornstalks 
themselves. 

§  408.  Symptoms.  The  insidious  nature  and  rapid 
course  of  the  disease  usually  result  in  the  death  of  the  animal 
before  its  presence  is  detected.  In  a  few  instances,  however, 
the  sick  animals  have  been  observed  very  carefully  by  their 
owners,  from  whom  all  of  our  knowledge  of  the  symptoms  is 
obtained.  One  owner  found  a  steer  lying  down  and  unable  to 
rise.  His  head  was  extended,  resting  on  the  ground  and 
moving  continually  from  side  to  side  ;  this  was  kept  up  for 
several  hours,  when  he  died.  In  the  second  place  a  steer  was 
found  to  remain  behind  the  other  animals  when  they  were 
driven  to  water  about  11  A.  M.  At  3  p.  m.  he  was  found  in  a 
dying  condition. 

Another  man  reported  that  he  found  his  animals  apparently 
well  at  5  A.  M.      At  7  A.  M.  a  heifer  was  found  resting  squarely 


MORHID    ANATOMY  521 

on  her  knees,  the  head  extended  and  resting  npon  the  ground. 
She  was  frothing  at  the  mouth  and  groaning  as  if  in  great 
distress.     She  died  in  about  two  hours. 

Another  report  states  that  the  sick  animals  were  dull, 
exhibited  great  weakness  and  walked  with  a  peculiar  jerky 
movement  of  the  hind  legs.  The  animals  trembled  as  if  suffer- 
ing from  a  chill.  In  a  short  time  they  fell  down  and  appeared 
to  be  in  great  distress,  heads  moving  continually  backward 
and  forward.  A  fourth  owner  observed  a  sick  animal  tremb- 
ling violently  for  al)0ut  two  hours  before  it  died. 

j^  409.  Morbid  anatomy.  In  twelve  animals  which 
died  in  cornstalk  fields  and  were  examined,  post-mortem 
changes  were  more  or  less  advanced  in  the  greater  number. 
A  few  were  examined  soon  after  death.  The  structural  changes 
in  the  organs  were  slight.  This  confirms  the  statement  of 
many  veterinarians  that  the  organs  of  the  cattle  dying  of  corn- 
stalk disease  are  normal  in  appearance. 

The  only  gross  pathological  changes  observed  were  those 
of  a  hemorrhagic  nature.  The  hemorrhages  were  mostly  con- 
fined to  the  serous  membranes  and  especially  those  of  the 
heart.  Ecchymoses  were  more  or  less  numerous,  however, 
beneath  the  pleura  and  under  the  capsule  of  the  liver  and  of 
the  spleen.  The  mucosa  of  the  intestinal  tract  showed  areas 
in  which  the  capillaries  were  deeply  injected.  Occasionally 
there  were  hemorrhages.  In  one  case  there  were  pronounced 
hemorrhagic  areas  in  the  heart  muscle,  aorta  and  pleura.  In 
most  cases  the  liver  was  pale  in  color  and  the  acini  presented 
deep  reddish  centers  with  pale  peripheries.  The  inner  and 
middle  zones  of  the  lobules  were  more  densely  congested  than 
the  peripheral  ones.  A  layer  several  lobules  in  thickness 
immediately  beneath  the  capsule  was  usually  more  engorged 
with  blood  than  the  deeper  portions  of  the  organ.  In  the 
more  densely  injected  areas  not  only  the  blood  spaces  were 
filled,  but  the  liver  cells  were  separated  from  each  other  by 
a  space  of  variable  width  containing  blood  corpuscles.  In 
some  cases  there  were  slight  changes  in  the  appearance  of  the 
cellular  protoplasm. 


522  CORNSTALK    DISEASE    IN    CATTLE 

In  all  of  the  animals  examined,  the  hemorrhages  were  of 
recent  origin  and  the  blood  normal  in  its  microscopic  appear- 
ance. There  were  no  discolored  areas  indicative  of  old  ecchy- 
moses.  The  distribution  and  general  character  of  the  hemor- 
rhages, which  are  the  most  conspicuous  microscopic  lesions 
observed,  are  ver}^  similar  to  those  described  in  certain  cases  of 
vegetable  poisoning,  more  particularh-  that  of  fern  root. 

Although  certain  symptoms  described  by  the  owners  were 
referable  to  the  nervous  system,  lesions  were  not  discovered  in 
the  brain  or  spinal  cord  excepting  in  one  case  in  which  there 
was  considerable  hemorrhage  beneath  the  pia  mater. 

In  one  animal  certain  of  the  lymphatic  glands  exhibited 
more  or  less  blood  extravasation,  particularly  in  the  interlob- 
ular tissue. 

<^  410.  Differential  diagnosis.  This  disease  is  to  be 
differentiated  from  sudden  deaths  from  accidental  causes, 
deaths  directly  due  to  engorgement,  or  to  the  consumption  of 
too  much  corn,  as  occasionally  happens  during  the  first  days 
that  the  cattle  are  in  the  stalk  field.  The  diagnosis  of  the 
cornstalk  disease  must,  for  the  present,  depend  upon  the  hem- 
orrhagic lesions  and  the  period  of  feeding  upon  the  stalks. 
Mayo  has  pointed  out  the  fact  that  occasionally  cattle  die  from 
eating  cornstalks  excessively  rich  in  nitrate  of  potash.  It  is 
not  impossible  that  the  hemorrhagic  lesions  are  those  of  .septi- 
cemia hemorrhagica.  The  only  argument  against  this  view  is 
the  negative  results  of  the  bacteriological  examinations  that 
have  been  made. 

Of  the  specific  infectious  diseases  which  might  be  confused 
with  the  affection,  acute  anthrax,  symptomatic  anthrax  and 
septicemia  hemorrhagica  should  be  mentioned.  Each  of  these 
affections  can  be  determined  by  its  specific  nature  as  pointed 
out  under  the  description  of  each  of  these  affections. 

REFERENCES. 

I.  BiLtiNGS.  The  cornstalk  disease  in  cattle.  Bulletins  Xo.  7,  S, 
9  and  10.     Neb.  Aoric.  Ex  per.  Station,  1886-S8. 


INFKCTIOUS    AHOKTION  523 

2  BiiiiNGS.  The  corn  fodder  disease  in  cattle  and  other  farm 
animals,  with  especial  relation  to  contagious  pleuro-pneumoma  m 
American  beeves  in  England.  BuUelins  No.  22  and  2:,.  C mv.  of  Nch. 
Agric.  Expcr.  Station,  1S92. 

7  i)K  ScHWKiNiTZ  Chemical  examination  of  cornstalks  presum- 
ably the  cause  of  cornstalk  disease  in  cattle.  Bulletin  No.  w,  U.  S. 
Bureau  of  Animal  Industry,  189b. 

4.  Gamgek.  Diseases  of  cattle  in  the  United  States.  U.S.  Pe- 
partmeint  of  Agriculture,  1869. 

5.  Mavo.  Cattle  poisoning  by  nitrate  of  potash.  Bulletin  No.  49. 
Kansas  A^rir.  l-lxper.  Station,  1895. 

6.  Mavo.     Cornstalk  diseases  in  cattle.     Ibid,  1896. 

7  MooRK  An  investigation  into  the  nature,  cause  and  means  of 
preventing  the  cornstalk  disease  (Toxemia  Maidis)  of  cattle.  Bnllettn 
No.  10,  U.  S.  Bureau  of  Animal  Industry,  1896. 


INFECTIOUS  ABORTION. 

^  411.  Characterization.  The  disease  or  condition 
known  as  infectious  abortion  consists  in  the  expulsion  of  the 
immature  fetus,  usually  before  it  has  sufficiently  developed  to 
live  after  birth,  by  a  large  proportion  of  pregnant  animals  that 
are  kept  together.  Usually  the  abortion  occurs  m  cattle  be- 
tween the  fifth  and  eighth  month  of  gestation.  The  disease 
as  described  bv  European  writers  is  characterized  by  certain 
morbid  changes  in  the  uterine  mucosa  and  fetal  membranes. 
American  observers  have  not  described  these  changes.  In 
cattle  it  usually  affects  the  young  cows.  After  two  or  three 
consecutive  abortions  cows,  as  a  rule,  become  immune  to  it. 
Cows  suffer  most  from  this  condition,  although  mares,  ewes, 
and  other  species  are  occasionally  reported  to  be  affected. 

In  Xorwav  infectious  abortion  is  scheduled  under  the  so- 
called  "milder  contagious  diseases."  Tlie  owner  is  obhged  to 
report  when  such  a  disease  appears  in  his  herd,  and  he  is  not 
allowed  to  bring  such  animals  to  fairs  or  cattle  shows. 

^  412.  History.  Abortions  in  epizootic  form  have  been 
recorded  from  very  early  times.      Mascal,  in  1S59.  .^ives  direc- 


524  INFECTIOUS    ABORTION 

tious  in  his  work  on  cattle,  "How  to  keep  cows  which  are 
great  bellied  with  calf."  In  Germany  the  disease  seems  to 
have  existed  in  a  somewhat  severe  form  in  the  latter  part  of 
the  eighteenth  century.  According  to  the  "Veterinary  Dic- 
tionary" (1897)  this  trouble  existed  in  Great  Britain.  The 
literature  on  animal  industry  and  agriculture  of  the  last  half 
century  contains  many  reports  of  the  existence  of  this  disease 
in  almost  every  cattle  raising  country.  The  most  important 
scientific  investigations  that  have  been  made  into  its  nature 
are  those  of  Nocard,  1885  ;  in  Great  Britain,  by  a  committee 
appointed  in  1886  by  the  Highland  Agricultural  Society  of 
Scotland  consisting  of  Drs.  Woodhead,  Aitken,  M'Fadyean 
and  Campbell;  and  in  Denmark,  by  Bang  and  vStreibolt.  Some 
work  was  done  on  this  disease  in  1897-98  at  the  New  York 
State  Veterinary  College  by  Law  and  Moore.  A  number  of 
the  State  Experiment  Stations  have  published  on  this  disease 
but  the  work  reported  has  been  more  in  the  line  of  treatment 
then  a  study  of  its  etiology. 

§  413.  Etiology.  Nocard  found  on  bacteriological  ex- 
amination of  cows  that  had  recently  aborted  two  different  species 
of  bacteria  present  in  large  numbers  in  the  purulent  substance- 
They  were  first  a  micrococcus,  found  abundantly  in  the  fluid 
lying  at  the  base  of  the  cotyledons  and  which  grew  either  singly 
or  in  short  chains.  The  second  was  a  short  thick  bacillus  which 
occurred  most  abundantly  in  the  juice  expressed  from  the 
follicles  of  the  cotyledons.  His  inoculation  experiments  were 
negative. 

Bang  and  Streibolt  found  an  anaerobic  bacillus  which 
possessed  somewhat  peculiar  properties  and  which  they  be- 
lieved to  be  the  specific  cause  of  the  disease.  They  found  it 
in  a  number  of  cases  and  report  positive  results  from  inocula- 
tion experiments.  The  cultivation  of  this  organism  required 
a  medium  composed  of  agar,  gelatin  and  blood  serum.  Bang 
considers  the  bacillus  he  discovered  to  be  a  purely  pathogenic 
organism  which  has  no  saprophytic  existence.  The  fact  that 
when  it  is  injected  into  the  blood  stream  it  grows  only  in  the 
pregnant  uterus  and  in  the  fetus  is  considered  evidence  of  this. 


MOK15ID    ANATOMY  525 

It  is  however,  able  to  live  for  a  long  time  outside  of  the  body. 
In  a'later  article  Bang  has  called  attention  to  the  intections 
nature  of  the  uterine  discharges  of  the  aborted  cows.  He 
believes  that  copulation  affords  the  most  favorable  opportunity 
of  all  for  infection. 

The  investigations  in  the  United  States  have  failed  to 
reveal  the  presence  of  Bang's  organism,  but  instead  a  variety 
of  B  coli  covtmnnis  has  been  found  by  Chester  and  by  Law 
and  Moore.  Nocard  showed  that  this  organism  is  able  to 
invade  the  uterus  and  provoke  the  expulsion  of  the  fetus. 

Lio-nieres,  reported  by  Nocard,  found  in  his  investigation 
that  the  cause  was  an  infection  of  the  mother  with  a  peculiar 
or-anism  constantly  present  in  the  digestive  tract.  Prior  to 
this  he  found  the  trouble  to  be  caused  by  the  secondary  inva- 
sion of  the  fetus  by  various  bacteria  that  are  always  recognized 
in  variable  numbers  in  raultiparous  cows. 

The    disappointing  part  of    these   investigations    ,s    that, 
with  the  exception  of  the  Americans  who  have  found  a  colon 
bacillus,  the  different  workers  have  not  verified   the  findings 
of  each  other.     Nocard  did  not  believe  that  abortion   was  due 
to  a    general    infection    of   the    dam,    because    the    cow    both 
immediately  before  and  immediately  after  the  act  of  abortion 
exhibits  no  svmptoms  of  disease  such   as  rise  of  temperature 
or  changes  in   the   urine,  blood  or   milk.     Smith   found  in  an 
epizootic  of  abortion  among  mares  a  bacillus  belonging  to  the 
hog-cholera  group  which  appeared  to  stand  in  an   etiological 
relation  to   the  trouble.     The  weight   of    evidence   seems   to 
indicate  that  this  form  of  abortion  is  caused  by  some  organism 
that  invades  the   uterus,  and  which  seems  to   be   transmitted 
from  the  infected  to  the  uninfected   animals  by    putting   them 
together  in  stables  and   in  some   instances   by   the  use  of  the 
same  bull. 

The  period  of  incubation   according  to   Bang  is  about    lo 

weeks. 

<  414.      Morbid  anatomy.     The  investigations  and  clin- 
ical observations   reported    in    this    country    have    not    called 


526  INFECTIOUS    ARORTION 

attention  to  any  definite  lesions  in  the  uterine  mucosa  or  fetal 
membranes  that  differ  materially  from  those  normally  found 
in  the  tissues.  Nocard  and  Bang,  however,  describe  very  pro- 
nounced changes.  Bang's  description  of  the  disease  is  as 
follows  : 

"  The  external  surface  of  the  uterus  was  normal.  The 
OS  uteri  was  firmly  closed  and  the  cervical  canal  was  filled  with 
the  normal  thick  mucus.  After  disinfection  of  the  serous 
covering  of  the  uterus  by  burning,  I  made  a  section  through 
the  uterine  walls  :  when  the  mucous  membrane  was  divided 
we  saw  between  that  and  the  foetal  envelope  an  abtindant  odorless 
exudate — a  dirty  yellow,  somewhat  thin,  pultaceous  material 
of  a  slimy,  somewhat  lumpy  character.  At  some  places  where 
the  fluid  constituents  had  run  out  the  exudate  was  of  a  semi- 
solid nature  ;  its  reaction  was  alkaline.  When  it  was  allowed 
to  stand  in  a  glass  it  separated  into  two  strata,  namely, 
superiorly  a  reddish  yellow  cloudy  serum,  and  at  the  bottom  a 
thick  greyish  yellow  precipitate. 

"  On  cutting  through  the  chorion  we  saw  under  that  a 
thin,  clear,  apparently  gelatinous  substance,  with  very  fine 
membranes  running  through  it  :  closer  examination  showed 
that  this  was  the  fine  connective  tissue  lying  between  the 
chorion  and  allantois,  saturated  with  oedematous  exudates. 
This  was  present  over  the  entire  extent  of  the  foetal  envelopes 
and  formed  a  layer  one  and  one-half  centimeters  thick.  The 
allantoic  fluid  was  natural  in  appearance,  thin^  yellowish,  and 
containing  fine  flocculi.  Nothing  abnormal  was  observable  iu 
connection  with  the  amniotic  fluid.  The  umbilical  cord  was 
oedematous.  The  size  of  the  foetus  and  degree  of  develop- 
ment of  the  hair  on  it  indicated  an  age  of  seven  months.  It 
was  quite  fresh  and  on  section  it  showed  no  striking  alteration. 
The  pericardium  contained  a  little  reddish  fluid  ;  the  intestinal 
mucous  membrane  was,  perhaps,  rather  redder  than  ordinary; 
the  spleen  was  in  very  slight  degree  swollen  and  the  blood  was 
fluid. 

"  The  examination  of  a  cover-glass  preparation  made  from 
the  yellowish  exudate  and  stained   with   Loeffler's   methylene 


MORHID    ANATCmV  527 

blue  immediately  showed  the  presence  of  a  very  small  bacter- 
ium, apparently  in  pure  culture.  This  organism  was  present 
in  very  considerable  numbers:  many  individuals  lay  free,  but 
most  striking  were  the  large  dense  clumps  of  bacteria.  Clo.ser 
examination  showed  that  the.se  heaps  were  included  within 
cells  whose  bodies  were  often  in  this  way  greatly  distended. 
Sometimes  the  body  of  the  cell  was  very  indi.stinct,  but  as  a 
rule  one  could  still  recognize  external  to  the  heap  a  part  of  the 
cell  body  and  often  also  the  cell  nucleus.  Not  seldom  the  cell 
body  had  assumed  a  peculiar  homogeneous  appearance. 

' '  In  the  dense  heaps  the  bacteria  mostly  had  the  appear- 
ance of  cocci,  but  some  of  the  free-lying  individuals  were  of  a 
longer  shape,  and  these  were  at  first  regarded  as  short  oval 
structures  ;  closer  examination,  however,  under  very  high 
magnification  showed  that  we  had  in  fact  to  deal  with  a  small 
bacillus  whose  body  contained  one,  two,  or  more  rarely  three, 
roundish  or  elongated  granules.  These  granules  most  readily 
took  up  the  stain.  The  length  of  the  bacillus  is  very  variable; 
the  longest  examples  are  about  as  long  as  tubercle  bacilli. 
.  The  granules  may  occur  a  little  distance  from  the 
extremities  but  frequently  they  are  at  the  end  of  the  bacillus. 
They  stain  with  the  ordinary  aniline  dyes,  but  not  by  the 
method  of  Gram.  The  bacilli  are  non- motile.  In  the  sub- 
chorial oedema  I  found  no  bacteria.  In  the  heart  blood  of  the 
foetus  there  were  a  few,  and  in  the  intestinal  contents  there 
were  many  staining  granules  ;  but  it  was  not  possible  to  say 
with  certainty  whether  these  were  bacteria  or  not." 

Bang  states  that  the  discovery  of  this  particular  organism 
indicates  that  epizootic  abortion  ought  to  be  regarded  as  a 
specific  uterine  catarrh,  determined  by  a  definite  species  of 
bacteria.  While  the  uterine  mucous  membrane  was  not 
strikingly  altered  he  affirms  that  chronic  catarrh  is  not  neces- 
sarily associated  with  striking  anatomical  alterations.  He 
states  further,  "  In  my  opinion  the  very  abundant  exudate 
which  contained  a  quantity  of  shed  epithelial  cells,  pus  cells 
and  detritus  must  necessarily  have  been  furnished  by  the 
uterine  mucous  membrane  and  not   bv   the  thin  chorion,   and 


528  INFECTIOUS    ABORTIOX 

consequeutly    the    disease    must    be    regarded     as    a     uterine 
catarrh." 

§415.  Prevention.  Dairyman  have  found  that  if  they 
keep  animals  that  abort  away  from  their  sound  cattle  the 
trouble  does  not  appear.  As  it  affects  young  cows,  it  is  the 
practice  in  some  places  to  keep  the  young  animals  separated 
from  the  others  until  they  have  become  free  from  the  disease 
or  at  least  until  they  have  passed  the  period  when  it  is  apt  to 
occur  after  which  they  are  admitted  to  the  herd  of  older  cows 
with  impunity. 

When  the  trouble  appears  in  a  herd  the  best  prophylactic 
is  thorough  disinfection  of  the  stable  and  frequent  washing 
with  a  disinfectant  of  the  vagina  and  external  genitalia  of  the 
cows  that  have  been  exposed.  The  vagina  and  uterus  of  the 
aborted  cows  should  be  thoroughly  washed  with  a  disinfecting 
solution.  Brauer  has  recommended  the  subcutaneous  injec- 
tion in  the  groin  of  twenty  grams  of  a  two  per  cent  solution  of 
carbolic  acid.  Immunizing  experiments  are  in  progress  under 
the  guidance  of  Professor  Bang,  but  it  is  too  early  to  speak  of 
the  results. 

All  new  cows  that  are  purchased  should  be  isolated  from 
the  herd  until  after  parturition  has  occurred  at  full  term. 

The  disinfectants  that  have  been  used  with  success  for 
external  application  are  5  per  cent  carbolic  acid,  4  per  cent 
creolin,  i  to  1000  corrosive  sublimate,  and  a  solution  of  copper 
sulphate  containing  fort}-  grams  per  liter  of  water.  The  last 
two  may  be  used  for  vaginal  douches.  Bang  recommends 
lysol  0.5  to  I  percent  for  this  purpose.  There  is  great  need 
of  further  investigation  into  the  control  of  this  affection. 

REFERENCES 

1.  Bang.  The  etiology  of  epizootic  abortion.  The  Jour,  of 
Camp.  Path,  and  Thera.,  Vol.  X  (1897),  p.  125. 

2.  Bang.  Infectious  abortion  in  cattle.  The  Jour,  of  Comp. 
Path,  arid  Thera.,  Vol.  XIX  (1906;,  p.  191. 

3.  Braner.  Ueber  das  Epizootische  Verkalben  der  Kiihe.  Deuts- 
che Zeitschrfur  Thier.,'&d.  XIV  (1888),  S.  95. 


VARIOLA  529 

4.  Chkstick.     Jill  annual  report,  Del.  Agric.  Exp.  Slaliou. 

5.  DAr.RVMiTvK.  Bullelin  No.  ro,  2ud  Series,  La.  Aj^r.  Exp. 
Station,  1891. 

6.  Gakdinkr.  Contagious  al)ortioii  in  Montana.  Iliilletin  No. 
fg,  Mon.  Aor.  Exp.  Station,  1903. 

7.  Kir.HORNK.  An  outbreak  of  abortion  in  mares.  lUillctiti  No. 
?,  V.  S.  Bureau  of  Animal  Industry,  1893,  p.  49- 

S.  Law.  Contagious  abortion  in  cows.  Report  of  the  N.  Y.  Stale 
Commissioner  0/  Agriculture,  1897. 

9.  Marshall.     Special  Bulletin  No.  13,  Mich.  Agr.  College,  1S99. 

10.  Nklson,  J.  Reports  of  the  Biological  Department  of  the  New 
I ersey  Agricultural  College  and  Experiment  Station,  1897,  1898  and 
"1899. 

11.  Nklsox,  S.  B.  /'ourth  Biennial  Report  of  the  State  I  eteri- 
narian  of  the  State  of  Washington,  1901  and  1902. 

12.  Xii.ivS.     Bulletin  No.  13,  Va.  Exp.  Station.  1902. 

13.  NoCARD.  Recherches  sur  I'avortment  epi/.ootique  des  vaches. 
Recueilde  Med.  I 'Her.,  VoL  III  (1886),  p.  669. 

14.  Pemberthy.  Epizootic  abortion,  four,  of  Comp.  Path, 
and  Thera.,  VoL  VIII  (1895),  p.  95-  (A  good  summary  of  the  history 
and  a  very  complete  list  of  references  to  the  earlier  literature  is  given.) 

15.  Smith.  On  a  pathogenic  bacillus  from  the  vagina  of  a  mare 
after  abortion.     Bulletin    No.   3.     Bureau    of  Animal  Industry,   1893,, 

P-  53- 

16.  Vanks.  Abortion  in  cattle.  Bulletin  No.  3  j.  North  Dakota 
Agricultural  College  and  Experiment  Station,  1902. 

17.  WooDHEAD  AND  OTHERS.  First  Report  of  the  Committee  of 
the  Highland  and  Agricultural  Society  of  vScotland.  Transactions  of 
the  Society  for  1887.  Second  Report  of  Committee.  Jour,  of  Comp. 
Path,  and  Thera.,  Vol.  II  (  1889),  p.  97- 


VARIOLA    IN    ANIMALS. 

Synonyms.  Variola  equinae:  hor.se  pox;  variola  vaccina: 
cow  pox;  variola  ovina;  sheep  pox;  variola  caprina;  goat  pox; 
variola  S7iilla;  swine  pox. 

iv  416.  Characterization.  The  disease  in  man  and 
animals  known. as  variola  is  characterized  by  a  rise  of  tempera- 
ture followed  l)y  a   skin   eruption   consisting   first   of   papules, 


530  VARIOLA 

then  of  vesicles  and  finally  of  pustules.  It  is  common  to 
horses,  cattle,  and  man.  Sheep  suffer  from  a  like  or  similar 
disease.     Other  species  are  said  to  be  occasionalh'  attacked. 

§  417.  History.  Small  pox  in  man  has  existed  from 
very  early  times.  It  is  reported  to  have  been  mentioned  in 
the  Chinese  records  of  11 22  B.  C.  It  was  quite  fully  and 
accurately  described  by  an  Arabian  physician  (Rhazesin)  in 
the  early  part  of  the  tenth  century.  The  disease  in  animals 
has  been  known  for  many  years.  Sheep  pox  is  reported  by 
Joubert  to  have  existed  in  1567.  Cow  pox  has  existed  for 
centuries  but  since  Jenner's  discovery  of  vaccine  it  has  received 
more  attention.     The  same  is  true  of  horse  pox. 

The  etiological  relations  of  the  pox  of  man  and  animals 
to  each  other  are  not  yet  clearl3'  enough  demonstrated.  The 
constantly  agreeing  anatomical  structure  and  the  like  develop- 
ment of  the  pustules  characteristic  of  the  disease  speaks  for  the 
etiological  identity  of  the  various  forms  of  pox,  but  yet  what 
we  know  concerning  their  different  infectiousness  especially 
the  susceptibility  to  them,  as  well  as  the  appearance  of  the 
disease,  accords  little  with  this  identity. 

While  in  man  and  sheep  the  disease  usually  appears  with 
severe  general  symptoms  and  with  a  diffuse  pock  eruption,  the 
eruption  is  confined  always  in  cattle  and  almost  always  in 
goats  to  single  places  on  the  body,  and  in  its  development  is 
accompanied  by  very  mild  general  symptoms.  The  disease 
among  men  on  the  one  hand  and  sheep  on  the  other  spreads 
very  easily,  providing  the  acquired  immunity  of  the  individual 
does  not  interfere,  while  on  the  contrary  among  other  animals 
the  spread  even  in  the  case  of  favorable  conditions  becomes 
important  only  within  narrow  limits. 

Doubtless  the  relations  between  the  pox  of  men  and  cattle 
are  very  close.  The  latter  is  ver}''  easily  inoculated  into  man 
yet  the  inoculation  always  produces  a  single  eruption  limited 
to  the  place  of  inoculation  and  never  a  general  affection  giving 
evidence  of  variola.  On  the  contrary  human  pox  is  much  less 
safely  transmitted  to  the  cow.  In  a  part  of  such  cases  there 
appear  in  the  cattle  characteristic  pocks  at  the  place  of  inocu- 


iiisTOKv  53  r 

lation,  in  other  cases  there  develops  after  the  inoculation  firm 
nodules  which  without  changing  to  vesicles  heal  without  scab- 
bing (Chauveau)  or  else  the  inoculation  remains  without 
results. 

The  experimental  evidence  seems  to  show  that  the  infect- 
ing element  of  human  variola  and  that  of  cows  (vaccina)  offer 
two  different  modifications  of  one  and  the  same  pox  contagion. 
Fischer  as  well  as  Eternod  and  Haggins  tried  also  to  prove 
this  by  the  fact  that  the  pox  lymph  inoculates  back  again  into 
man  after  which,  in  many  thousands  of  people  inoculated  in 
this  manner,  only  a  local  pox  eruption  developed.  The  above 
named  authors,  as  well  as  RolofT  and  Bollinger,  draw  the  con- 
clusion from  this  that  variola  in  its  transmission  through  the 
bodies  of  cattle  changes  to  vaccinia  and  that  the  latter  there- 
fore presents  nothing  but  a  weakened  modification  of  the  first. 
That  this  change  does  not  always  take  place  easily  and  in  the 
above  mentioned  way  is  shown  by  the  experiments  of  Chau- 
veau, who  after  inoculating  with  the  lymph  taken  from  cows 
inoculated  with  variola  saw  the  pox  repeatedly  appear  in  men 
as  a  severe  general  disease. 

The  very  close  relationship  between  human  variola  and 
vaccina  is  shown  through  the  fact  that  the  vaccine  produces  a 
lasting  immunity  to  the  variola.  Since  the  local  illness  in 
man  following  vaccination  is  a  mild  form  of  human  pox,  vac- 
cine must  be  considered  as  a  weakened  form  of  variola  virus. 
If  one  considers  further  that  the  transmission  of  the  contagion 
from  person  to  person,  as  such  inoculations  were  usual  in  the 
past,  in  most  cases  produced  only  a  local  lesion,  so  that  in 
cattle  the  pox  as  a  rule,  perhaps  almost  always,  appeared  as  a 
result  of  the  transmission  of  the  virus  from  a  person  sick  with 
inoculation  pox,  the  conclusion  is  well  founded  that  the  con- 
tagion of  cow  pox  really  presents  a  weakened  modification  of 
the  human  pox  virus. 

Jenner  was  of  the  opinion  that  cow  pox  appeared 
as  a  result  of  infection  by  horses  sick  with  pox  and  therefore 
concluded  that  it  was  identical  with  cow  pox.  Later  Lafos.se 
and  afterwards  Bouley  agreed  with  this  opinion       Under  the 


532  VARIOLA 

influence  of  the  authority  of  the  latter  author  as  well  as  of 
Chauveau,  this  conception  was  commonly  received  in  France 
until  recently  Warlemont  and  Hugues  discovered  that  the 
horse  is  slightly  susceptible  to  vaccine.  Dieckerhoff  and 
Rawitz  have  made  the  assertion  that  the  contagious  disease 
observed  by  certain  of  the  former  authors  was  not  pox  sickness 
but  sometimes  stomatitis,  and  sometimes  dermatitis  contagiosa 
pustulosa,  which  latter  diseases  are  transmissible  to  other  kinds 
of  animals  as  well  as  to  cattle. 

Sheep  pox  as  a  result  of  natural  infection  usually  spreads 
exclusively  to  sheep,  not  being  transmitted  to  the  closely 
related  goats,  and  it  is  not  dangerous  to  man.  Human  pox  is 
only  rarely  inoculated  into  sheep.  Efforts  to  immunize  cattle 
with  the  contagion  of  sheep  pox  against  cow  pox  have  not 
been  successful.  According  to  Pound  the  sheep  pox  must  be 
considered  as  a  specific  disease  of  sheep.  The  same  conclu- 
sion has  been  entertained  relative  to  goat  pox. 

The  pox  of  other  species  of  animals,  as  far  as  they  gen- 
erally appear,  manifest  themselves  in  consequence  of  an  epi- 
demic in  man  or  an  epizootic  in  one  of  the  species  of  animals 
and  therefore  cannot  be  considered  as  independent  forms  of 
the  disease. 

According  to  our  present  knowledge  human  pox,  .sheep 
pox  and  goat  pox  present  symptoms  independent  of  each  other 
in  their  beginning  and  spread,  while  the  pox  of  the  other 
species  of  animals  always  stand  in  a  casual  relation  to  one  of 
the  cited  forms  of  disease.  But  this  conception  does  not  agree 
completely  with  the  relationship  of  these  forms  of  disease.  On 
the  contrary  the  present  agreement  in  the  development  of  the 
otherwise  specific  pathological  process  makes  the  opinion 
probable  that  the  pox  disease  was  a  specific  entirely  independ- 
ent disease  of  one  of  the  mentioned  species  of  animals  or  of 
man  which  was  also  transmissible  to  other  species  of  animals  ; 
but  in  the  course  of  time  the  virus  has  passed  through  several 
generations  of  different  species  of  animals  and  has  become 
adapted  to  the  life  conditions  in  the  bodies  of  the  different 
species  of  animals.     As  a  result  of  this  the  virus  thus  living  in 


SV.MFTOMS  533 

one  species  lost  parti >•    or   entirely    its  pathogenesis   for  other 
species. 

^  418.  Geographical  distribution.  It  has  been  re- 
ported in  animals  from  many  places  in  Kurope,  in  northern 
Africa  and  Asia.      Cow  pox  has  been  reported  in  America. 

v^  419.  Etiology.  The  cause  of  variola  is  not  known. 
A  number  of  different  microorganisms  have  been  isolated  but 
thus  far  their  discoverers  have  not  been  able  to  reproduce  the 
disease  with  them.  Some  investigators  believe  the  cause  to 
be  a  protozoan  which  they  believe  they  have  found  in  the  tis- 
sues. The  work  of  Councilman  stands  foremost  in  this  line. 
The  virus  is  quite  hardy  and  remains  alive  for  a  considerable 
time  if  not  exposed  to  direct  sunlight.  The  identity  of  the 
disease  in  horses,  cattle,  sheep  and  man  has  not,  therefore, 
been  positively  determined,  although  the  results  reported  by 
Hine,  Simpson,  Freyer  and  others  suggest  an  etiological  rela- 
tionship if  not  an  identity.  If  the  identity  is  not  established, 
then  the  diseases  in  the  different  species  now  called  variola 
must  be  considered  as  distinct  maladies.  It  seems  desirable 
at  this  time  to  consider-them  under  the  generic  name  l^ariola, 
treating  the  disease  as  found  in  each  species  separately. 

§  420.  Symptoms.  The  symptoms  vary  .somewhat  in 
the  different  species,  but  the  essential  ones  are  a  rise  of  tem- 
perature and  the  appearance  of  a  definite  eruption  on  the  skin 
or  mucous  membranes.  This  is  at  first  papular,  then  vesicular 
and  finally  pustular.  It  is  rarely  a  dangerous  affection  in 
animals  and  often  it  is  very  mild.  The  peculiar  symptoms 
and  lesions  as  recognized  in  each  species  of  animals  are 
appended. 

Ji  421.  Horse  pox.  The  eruption  occurs  on  the  buccal 
membrane,  nasal  mucosa,  conjunctiva  (rarely),  mucosa  of 
generative  organs,  and  upon  the  skin.  In  the  latter  case  the 
pustules  may  occur  over  the  entire  body  or  be  localized  in 
certain  regions.  The  lesions  consist  of  the  specific  pustules. 
On  the  mucosae  the  pustule  begins  with  the  congestion  of  the 


534  VARIOLA 

skin  followed  b}-  an  initial  ecchymosis  and  occasional!}'  by  an 
abundant  exudate,  The  mucosa  becomes  opaque.  The  liquid 
accumulates  in  vesicles  followed  by  a  pustular  condition  with 
a  crust  or  scab  covering  it.  Upon  the  skin  the  eruption  is 
characterized  by  ecchymosis  with  marked  hyperemia.  The 
histological  changes  have  not  been  fully  described.  The  des- 
criptions published  appear  to  be  copied  from  those  of  human 
small-pox. 

§  422.  Cow  pox.  In  the  bovine  species  the  eruptions 
are  usually  on  the  skin  of  the  teats  or  udder.  Other  parts  are 
said  to  be  occasionally  involved.  The  period  of  incubation  is 
said  to  be  about  two  days  after  inoculation.  The  first  symptom 
is  a  tenderness  of  the  skin  of  the  teats  or  udder,  then  follows 
the  appearance  of  small  reddish  spots.  A  few  days  later  these 
become  vesicles,  then  pustules  with  a  depressed  umbilicated 
center.  These  are  surrounded  by  a  pinkish  or  reddish  areola. 
The  pustules  crust  over  in  a  few  days  leaving  a  scab  several 
millimeters  in  diameter.  Usually  many  of  the  vesicles  are 
ruptured  by  the  hands  of  the  milker.  This  often  leads  to  scars 
that  heal  with  difficulty.  It  may  happen  that  eruptions  in  all 
the  stages  of  development  may  appear  on  the  teats  at  the  same 
time. 

The  diagnosis  of  cow  pox  depends  on  the  presence  of 
regular  pustules  with  a  depression,  and  in  many  cases  a  similar 
exanthema  on  the  hands  of  the  persons  occupied  in  the  caring" 
for  the  affected  animals.  The  injuries  and  irritations  caused 
by  milking  makes  the  diagnosis  more  difficult.  It  is  possible 
to  confuse  it  with  the  exanthema  of  foot  and  mouth  disease, 
although  here  the  nodules  do  not  develop  into  pustules  and 
are  at  the  same  time  larger  and  less  regularly  formed  and  there 
are  besides  that  similar  vesicles  even  in  the  mouth  and  the 
split  of  the  hoof  of  the  sick  animals.  The  mild  eruption  of 
vesicles  is  easy  to  recognize  in  the  simultaneous  affection  of 
the  genitals.  In  rinderpest,  pustules  are  also  sometimes  formed 
on  the  vidder,  but  this  appearance  is,  in  comparison  with  other 
general  and  local  symptoms,  of  slight  importance. 


SHEKP   POX  535 

ij  423.  Sheep  pox.  This  affection,  known  diSclavclee,  is  an 
acute  febrile  disease  of  sheep  and  goats  occurring  epizootically 
and  existing  in  enzootic  form  in  certain  parts  of  Europe, 
Africa  and  Asia.  It  is  usually  not  fatal  but  a  mortality  of 
from  7  to  20  per  cent,  according  to  the  outbreak,  is  reported. 
It  is  marked  by  a  rise  in  temperature  and  general  disability 
followed  by  the  appearance  of  a  series  of  changes  on  the  bare 
and  merely  hairy  portions  of  the  skin.  These  consist  of 
papules,  vesicles  and  pustules  which  are  later  covered  with  a 
scab.  They  dry  up  and  drop  off  in  from  15  to  20  days. 
Observers  have  distinguished  two  forms  of  this  affection  in 
sheep,  namely,  a  discrete  form  and  a  confined  variety.  There 
may  be  hemorrhages  giving  the  dark  or  black  sheep  pox. 

Borrell  found  that  when  the  scraping  from  a  pustule  was 
suspended  in  water  (mixed  )  it  remained  virulent  after  much 
dilution.  When  this  suspension  was  filtered  through  a  Berke- 
feld  cylinder  the  filtrate  was  still  virulent.  It  did  not  pass 
through  a  Chamberland  filter  F.  The  filtrate  retains  its  viru- 
lence for  a  long  time.  Borrell  considers  that  his  results  show 
that  the  microbe  of  sheep  pox  is  ultra  microscopic  and  that 
the  cellular  inclusions  described  as  parasites  of  vaccinia,  of 
variola,  of  davelee,  cannot  be  the  true  cause  of  the  disease. 
He  believes  that  the  researches  should  be  directed  along  the 
lines  of  those  made  in  connection  with  contagious  pleuro- 
pneumonia and  foot  and  mouth  disease. 

Pathogenesis.  x-Vccording  to  Hutyra  and  Marek  the 
cutaneous  inoculation  of  a  small  drop  of  pox  lymph  usually 
causes  in  susceptible  sheep  only  a  local  pox  eruption  ;  in  part 
of  the  cases,  however,  especially  in  lambs  or  when  very  virulent 
lymph  is  used,  there  also  appears  a  general  pox  eruption.  In 
the  latter  case  there  forms  at  the  place  of  inoculation  after 
2-2  >^  days'  incubation  a  dark  red  nodule  which  softens  in 
from  four  to  five  days  and  changes  into  a  vesicle.  The  latter 
attains  the  size  of  a  dollar,  its  top  later  sinks,  from  the  interior 
a  little  lymph  oozes  out  which  later  becomes  thick,  until  on  the 
1 2th  or  13th  day  after  the  inoculation  a  scab  forms  with  a 
gradual    drying  of    the    pox    content.       With    the  beginning 


536  VARIOLA 

of  the  softening  of  the  nodule  the  body  temperature  rises  to 
39.5-40.6°,  later  to  41.5-42.6°  as  a  sign  of  the  entrance  of  the 
virus  into  the  circulation,  in  consequence  of  which  nodules 
form  on  the  mucous  membrane  of  the  lips,  around  the  nose 
and  eyelids,  later  also  in  the  axillary  region,  on  the  thighs,  in 
the  pubic  and  anal  regions.  Later  these  form  into  pock  vesicles. 
At  the  same  time  the  general  symptoms  of  fever  reach  a  high 
grade  until  at  the  beginning  of  the  third  week  after  infection 
or  perhaps  later  death  follows  with  symptoms  of  septicemia. 
After  subcutaneous  infection  the  temperature  rises  with  the 
beginning  of  the  local  inflammation  ;  the  latter  consists  of  a 
hard  swelling  the  size  of  a  fist,  with  countless  nodules,  later 
with  pock  vesicles  running  together  on  the  surface,  while  the 
pock  eruption  generally  follows  on  the  5th  or  6th  day  after  the 
infection  and  in  a  manner  similar  to  that  after  cutaneous 
inoculation.  Intraperitoneal  injection  of  the  lymph  results 
directly  in  the  formation  of  nodules  on  the  peritoneum  with 
swelling  and  painfulness  of  the  abdomen,  a  specific  inflamma- 
tion of  the  mucous  membrane  of  the  trachea  with  exceedingly 
difficult  breathing,  to  which  is  generally  added  a  general  pock 
eruption  on  the  6th  or  8th  day  (Bosc).  Injection  of  the  lymph 
into  the  circulation  generally  causes  a  rise  of  temperature 
without  skin  eruption,  but  though  the  disease  is  slight  and  of 
short  duration  the  sheep  become  as  immune  as  after  surviving 
the  typical  disease  (Semmer  and  Raupach) .  After  intracerebral 
inoculation  fever  occurs  after  6  or  8  days,  upon  which  the 
animals  die  within  a  week,  while  injection  of  the  lymph  into 
the  lactiferous  duct  causes  a  pock  eruption  on  the  mucous 
membrane  of  the  udder  and  the  milk  contains  the  infective 
material  for  two  weeks  (Nocard). 

Natural  infection.  The  contagion  of  sheep  pox,  which 
usually  comes  in  the  form  of  a  general  disease,  according  to  all 
probability  reaches  the  lungs  with  the  inspired  air  and  here 
passes  from  the  alveoli  directly  into  the  blood,  by  which  it  is 
carried  to  the  superficial  vessels  of  the  skin  and  mucous  mem- 
brane. By  injection  or  spraying  of  the  pock  lymph  into  the 
trachea  of  susceptible  sheep  the  disease  is  sure  to  be  reproduced. 


GOAT   POX  537 

while  feeding  of  the  lymph  is,  according  to  Hicard,  ineffective. 
Rickert  has  inoculated  about  700  sheep  in  the  last  week  of 
pregnane}'.  Repeated  inoculations  of  the  lambs  born  of 
them  remained  negative  while  of  36  lambs  from  others  not 
inoculated  pox  occurred  9  days  after  the  inoculation.  After 
three  years  inoculations  in  the  case  of  the  former  had  positive 
results  but  in  the  latter  no  longer.  In  the  same  way  Adacker 
has  inoculated  60,  Peuch  3,  lambs  born  of  sick  mothers  without 
any  result  (the  latter  also  3  kids). 

424.  Goat  Pox.  J^aiiola  caprina.  The  goat  pox  was 
formerly  observed  in  Sweden.  It  has  been  found  in  Italy, 
Spain,  France,  Germany  and  in  Algeria.  It  has  been  reported 
that  in  Algeria  it  is  occasionally  very  severe. 

Etiology.  The  contagion  of  goat  pox  can  be  transmitted  to 
goats  through  the  pock  content  and  when  the  pustules  are  in 
the  mouth  through  the  saliva  of  the  sick  animals.  After 
cutaneous  inoculation  a  local  eruption  develops  at  the  place  of 
inoculation  associated  with  very  mild  general  symptoms.  Man 
is  not  entirely  unsusceptible,  as  there  appears,  especially  on  the 
hands  and  arms  of  people  who  care  for  the  sick  goats,  an 
exanthema  with  little  vesicles  (Hansen,  Marcone). 

Natural  infection  takes  place  by  direct  touch  and  the 
disease  in  this  way  spreads  quickly  into  the  herd  of  goats  so 
that  as  a  rule  almost  all  the  animals  are  infected  (sheep  kept 
with  the  goats  are  never  affected).  On  the  other  hand  the 
disease  shows  no  inclination  to  spread  to  wider  territories  but 
usually  stays  confined  to  one  herd. 

The  manifestation  of  the  disease  is  very  similar  to  the 
sheep  pox.  In  connection  with  a  moderate  fever  there  develops 
large  pustules  partly  confluent  and  with  a  depression,  on  the 
most  diverse  parts  of  the  body,  especially  on  the  udder,  the 
inner  surface  of  the  extremities,  the  face  and  around  the  lips 
and  eyes.  These  leave  radiating  scars.  In  many  cases 
abscesses  form  in  the  tissues  of  the  udder,  and  at  the  same 
time  the  milk  becomes  bloody.  In  certain  animals,  especially 
nursing  kids,  there  also  appear  in  the  mouth,  as  well  as  in  the 


538  VARIOLA 

mucous  membrane  of  the  upper  air  passages,  lesions  whose 
development  is  accompanied  by  coughing,  rapic  breathing  and 
a  pus-like  discharge  from  the  nose. 

The  prognosis  of  the  disease  is  generalh'  favorable  :  at  the 
site  of  the  confluent  pustules  the  skin  sometimes  dies  and 
sloughs  out,  which  retards  convalescence.  In  very  few  cases 
the  disease  develops  a  severe  form  from  the  beginning  and  is 
accompanied  by  general  infection  and  death. 

This  affection  may  be  confused  with  foot  and  mouth  disease 
because,  according  to  Conte,  in  goats  the  pustules  of  the  pox 
.sometimes  reach  considerable  size  ;  however,  the  characteristic 
appearance  of  the  pox  exanthema  as  well  as  the  fact  that  the 
claws  remain  unaflfected,  and  the  inability  to  transmit  it  to  other 
animals,  will  prevent  a  mistake  in  diagnosis. 

^  425,  Swine  pox.  The  occurrence  of  swine  pox  is  not 
yet  determined  with  positiveness.  Because  in  common  parlance 
all  sorts  of  skin  eruptions  of  swine  are  designated  as  pox  the 
characteristic  nature  of  many  diseases  described  under  this 
name  is  doubtful.  After  Chauveau  has  transmitted  cow  pox  in 
single  cases  to  sheep.  Gerlach  swine  pox  to  goats,  and  Koch 
swine  pox  to  calves,  the  occurrence  of  swine  pox  cannot 
reasonably  be  doubted  and  it  is  also  probable  that  the  disease 
passes  from  the  cow,  from  man  and  perhaps  also  from  the  goat 
to  swine,  and  once  occurring  easily  spreads  among  the  animals 
turned  together.  According  to  the  descriptions  the  disease  as 
a  rule  attacks  only  young  pigs  and  for  the  most  part  manifests 
itself  in  an  exanthema  spread  over  the  greater  part  of  the  body. 
Several  days  after  its  appearance  the  animal  shows  signs  of 
weakness,  loss  of  appetite,  slow  movements,  stiff  walk,  tail 
hanging  straight  down,  shivering  and  ruffled  bristles.  There 
immediately  appear  on  the  parts  of  the  body  with  little  or  no 
hair,  such  as  the  nose,  the  eyelids,  the  inner  surface  of  the 
thighs,  the  abdomen,  seldom  on  the  neck  and  back,  little  red 
marks  which  quickly  increase  in  size.  In  the  center  of  these 
there  develops  firm  nodules  and  after  two  or  three  days  the 
latter  develop  into  pox  the  average  size  of  a   pea  and  filled  at 


El'ITHKLIOMA    CONTAGIOSUM  539 

first  with  pure  lymph,  later  with  pus;  these  shortly  dry  to  dark 
brown  scabs  which  fall  off  after  a  few  days.  In  more  severe 
cases  the  pustules  became  confluent. 

The  diagnosis  between  this  affection  and  the  different 
forms  of  eczema,  erysipelas  and  urticaria  is  not  easy.  There 
is  much  need  of  further  investigation  of  this  group  of  diseases. 

RKFKRKNCKS. 

1.  Bkrrv.     Contagious  pustular  dermatitis  of  sheep. 

2.  BoRRKL.  Htude  experimentale  de  la  clavelee  filtration  da 
virus;  Sero-clavelisation  ;  vSerotherapie.  ^lini.  de  Tlnst.  Pasteur,  \o\. 
XVri  I  1903),  p.  123. 

3.  Councilman,  Macrath  and  Brinckerhoff.  The  patho- 
logical anatomy  and  histology  of  variola.  The  Journal  of  Medical 
Research,  \o\    W  (1904),  p.  12. 

4.  DuPiTis.  Colques  cas  de  cow-pox  :  Eruption  generalisee. 
Auuahdc  Med.  I'el.,  1889,  p.  18  ^ 

5.  EilHRTS  dk  Haan.  Vaccine  et  retrovaccine  a  Balavia.  Amia/s 
deriusf    Pasteur,  1896,  p.   169. 

6.  Hi^iK.  Successful  transformation  of  small-pox  into  cow-pox. 
British  Medical  Journal,  1892,  p.    i  16. 

7.  NOCARD.  Etudes  experimentales  sur  la  clavelee.  Bulletin  de 
la  Societe  Cent.  Med.  I'et.,  1899,  p.  263. 

8.  .Simpson.  Vaccinia  produced  by  passing  the  vaccine  of  small- 
pox.    Indian  Medical  (lazette,  1896,  p.  205. 


EPITHELIOM.'\  CONT.\(tIOvSUM. 

Synonyms.      Chicken  pox  ;   la  petite  verole;  sore  head. 

^  426.  Characterization.  Epithelioma  contagiosum, 
or  chicken  pox  as  it  is  more  commonly  called  in  this  country, 
is  characterized  by  the  development  of  nodular-like  growths 
upon  the  mucosa  and  skin  of  the  head  and  neck.  It  is  readily 
transmitted  among  fowls.  Other  birds  especially  pigeons  are 
said  to  be  affected. 

i^  427.  History.  This  affection  of  fowls  has  been  known 
for  a  long  time.      It  was  thought  in  early  times  that  it  was  re- 


540 


EPITHELIOMA    CONTAGIOSUM 


lated  to  small  pox.  Spinola  failed  to  produce  it  in  fowls  with 
cow  pox.  In  1873,  Bollinger  gave  a  very  full  account  of  his 
investigations  into  its  nature. 

^  428.      Geographical  distribution.      This  affection   has 
been  studied  in  Europe.      In  the  United  States,  Salmon  refers 


Fig.  121.     A  photograph  of  the  head  of  a  fowl  shonnng  epithelioma  on 
the  coinh  and  in  front  of  the  eye  {after  Ward). 


to  it  from  the  Southern  States  and  Ward  has  described  it  in 
California.  Sedgwick  reports  that  it  is  one  of  the  greatest 
obstacles  to  chicken  raising  in  Hawaii. 

^  429,      Etiology.      The  cause  of  this  disease  is  not  satis- 
factorilv  settled.      Rivolta  and  Silvestri  considered  coccidia  to 


SYMPTOMS  541 

be  the  exciting  cause.  The  disease  is  readil\-  transmitted  by 
inoculation.  Ward  has  ])roduced  it  by  simply  pricking  the 
tumor  with  a  syringe  needle  and  then  puncturing  the  skin  on 
the  head  of  a  healthy  chicken  Marx  and  Stickler  ground  up 
the  tumors  or  nodules  in  normal  salt  solution  and  passed  this 
through  a  Berkefeld  cylinder.  The  filtrate  rubbed  on  the 
scarified  combs  of  healthy  chickens  produced  the  disea.se.  The 
virus  did  not  pass  through  the  porcelain  filters. 

§430.  Symptoms.  The  disease  first  manifests  it.self  by 
a  catarrh  of  the  mucosa  of  the  head.  In  the  further  course 
of  the  disease  wart-like  proliferations  appear  on  the  mucosa 
and  extend  to  the  skin.  The  epitheliomata  are  usually  at 
first  gray  and  glistening  but  later  they  are  covered  with  a  scab. 
The  nodules  may  become  so  numerous,  or  if  single  so  large, 
that  the  eyes  are  closed,  in  which  case  the  fowls  being  unable 
to  see  may  die  from  starvation.  The  growths  ma}^  also  inter- 
fere with  the  use  of  the  beak.  The  lesions  are  usually  local 
on  the  unfeathered  part  of  the  head.  They  are  said  at  times 
to  extend  to  the  feather  covered  skin.  The  affected  fowls  are 
used  for  food  unless  there  are  objectionable  secondary  changes 
resulting  from  lack  of  ability  to  eat.  Recovery  often  takes 
place  in  from  three  to  four  weeks. 

§  431.  Morbid  anatomy.  The  nodules  consist  of  epi- 
thelial cells.  There  is  a  cell  infiltration  of  the  skin  and  sub- 
cutaneous tissue.  The  epithelial  cells  are  much  larger  than 
normal;  they  may  be  in  scales  or  in  more  dense  masses.  Later 
in  the  course  of  the  disease  the  nodules  may  drop  off  as  scales. 

RHFERENCES. 

1.  BOLT^iNGER.  Ueber  EpitheHoma  contagiosa  beim  Haushuhn 
iind  die  sogenannten  Pocken  des  Gefliigels.  Archiv.  fi'ir.  Path.  AnaL, 
Bd.  LVIII  (1873),  S.  349- 

2.  Heusixger.  Reclicrches  de  Path.  Coiiif>.,  Vol.  i,  (1847), 
p.  649. 

3.  Salmon.     Diseases  of  Poultry . 

4.  Sedgwick.  Chickens  and  their  diseases  in  Hawaii.  Piilleiin 
No.  /,  Hcnvaii  Agric.  Expt.  Station,  1901. 


542  INFECTIVE    SARCOMATA 

5.  Spinola.     Handbuch    der.  spec.  Pai/i.   u.       Thera.  fiir.    Thie 
rarzte,  1858. 

6.  Ward.     Poultry    diseases    in    California.     Proceedings   of  the 
Am.   Vet.  Med.  Asso  ,  1904,  p.  164. 


INFECTIVE  SARCOMATA   IN   DOGS. 

§432.  Infective  sarcomata  in  dogs.  Smith  and  Wash- 
burn have  described  a  series  of  tumors  of  dog.s  which  spread 
from  animal  to  animal  as  the  result  of  coitus.  These  tumors 
which  varied  much  in  size  appeared  to  start  in  the  mucosa  of 
the  vagina.  In  some  cases  the  walls  of  the  vagina  were 
deeply  infiltrated,  and  the  tumors  often  ulcerated.  Death 
occurred  frequently  from  cachexia  or  as  the  results  of  mechani- 
cal obstruction.  They  were  enabled  to  successfully  inoculate 
the  tumors  into  two  dogs.    The  following  are  their  conclusions: 

1.  "The  tumors  in  question  are  infective  round  celled 
sarcomata  occurring  in  dogs. 

2.  "The  tumors  can  be  transplanted  from  the  genitals, 
where  they  naturally  occur,  to  the  subcutaneous  tissue  of  dogs. 

3.  "The  tumors  can  be  transplanted  from  subcutaneous 
tissue  to  subcutaneous  tissue  through  a  series  of  dogs. 

4.  "The  tumors  after  reaching  the  maximum  of  growth 
may  disappear  spontaneously  with  or  without  ulceration. 

5.  "The  tumors  may  continue  to  increase,  and  may 
cause  death  by  secondary  deposits  forming  in  the  viscera. 

6.  If  the  tumor  should  disappear  the  animal  is  then 
immune  to  subsequent  inoculation." 

Beebe  and  Ewing  have  studied  these  nodular  tumors. 
They  have  been  able  to  transplant  it.  From  122  plants  by 
various  methods  they  have  produced  tumors  in  35  cases  and 
there  were  12  spontaneous  recoveries.  The  course  of  the 
successful  implantations  is  usually  quite  uniform.  When 
inserted  beneath  the  skin  a  period  of  2  to  3  weeks  elapsed 
before  enlargement  was  noticed.  Thereafter  the  nodules  grew 
steadily  in  size  for  four   or    five    months    producing    a    well- 


SYMPTOMS  543 

circumscribed  tumor  the  size  of  a  hen's  egg  or  larger.  These 
authors  did  not  determine  the  histological  classification  of  the 
tumor. 

REFERENCES 

1.  Beebe  and  Ewing.  a  stud}-  of  the  so-called  infectivus  lym- 
phosarcoma of  dogs.  The  /our.  Med.  Research,  Vol.  XV  (1906)^ 
p.  209. 

2.  Smith  and  Washburn.  British  Medical  Journal,  Dec.  17. 
1908. 

FOWL  PEST. 
Synonyms.       Vogelpcst;  Huhner-pest;  exudative  typhus. 

§  433.  Characterization.  This  is  a  very  acute  and 
rapidly  fatal  disease  of  fowls  caused  by  an  ultra-microscopic 
organism  that  passes  through  the  Berkefeld  and  Chamberland 
filters.  Pigeons  succumb  to  inoculation.  Guinea-pigs  and 
mice  are  susceptible. 

§  434.  History.  In  iSSo,  Rivolta  and  Delprato  differ- 
entiated a  disease  from  chicken  cholera  which  they  designated 
''exudative  tj-phus."  Perroncito  called  it  a  typical  fowl 
cholera.  It  was  investigated  and  described  by  Lode  and 
Gruber  in  1901.  It  was  found  in  the  Tyrol  where  during  the 
time  from  March  until  July  it  had  attacked  2,300  hens  with  a 
mortality  of  from  80  to  95  per  cent.  Centanni  described  this 
disease  and  the  nature  of  its  virus.  He  states  that  it  has  been 
recognized  as  a  distinct  affection  for  more  than  ten  years. 

§  435.  Geographical  distribution.  It  has  appeared  in 
Belgium  and  the  Tyrolean  Alps  and  a  few  other  places  in 
Europe. 

§  436.  Etiology.  This  disease  appears  to  be  due  to  an 
invisible  microorganism.  The  blood  or  aqueous  suspension 
of  crushed  lungs  or  liver  will  usually  produce  the  disease  when 
injected  in  very  small  doses.  It  was  found  by  Maggiora  that 
4  cc.  of  a  dilution  of  virulent  blood  in  which  the  blood  was 


544  FOWL    PEST 

present   in  the  proportion    of    i    to    125,000,000    destroyed    a 
young  hen. 

The  virus  retained  its  virulence  in  blood  for  15  davs.  It 
was  destroyed  in  thirty  minutes  at  a  temperature  of  60°  C. 

§  437-  Symptoms.  According  to  Centanni  the  chicken 
acts  dumpish  the  first  day  and  refuses  food  on  the  second. 
The  feathers  are  ruffled,  the  comb  discolored  and  on  the  third 
day  it  dies.  More  rapidly  fatal  cases  are  mentioned  by  Lode 
and  Gruber.  The  temperature  is  at  first  high  but  it  falls  to 
subnormal  before  death. 

ij  438,  Morbid  anatomy.  The  lesions  vary.  In  some 
cases  death  follows  so  rapidly  that  autopsies  reveal  no  change. 
Usually  there  is  a  slight  pericarditis  and  ecchymoses  in  the 
heart  muscle.  There  is  pleurisy  in  some  cases.  The  lungs 
are  congested  and  occasionally  there  are  pneumonic  centers. 
The  liver,  spleen  and  kidneys  are  more  or  less  congested. 
Microscopic  changes  are  not  described. 

§  439.  Differential  diagnosis.  This  is  to  be  differen- 
tiated from  fowl  cholera  and  typhoid.  The  diagnosis  is  made 
from  the  bacteriological  examinations.  The  rapid  cour.se  of 
the  disease  cannot  be  relied  upon  as  a  differential  character, 
for  both  fowl  cholera  and  fowl  typhoid  often  run  very 
rapid  courses  and  likewise  have  a  high  mortality. 

REFERENCES. 

1.  Centanni.  Die  Vogelpest  ;  Beitrag  zu  dem  (lurch  kerzen 
filtrirbaren  Virus.      Cent.  f.  Bakt.     Bd.  XXXI  (1902),  vS.  145.  u.  182. 

2.  Dubois.  Une  maladie  infectieuse  des  poules  a  microbes  invisi- 
bles.    Coinp.  Rend.  Soc.  de  biol.     Vol.  LH'  (1902),  p.  1162. 

3.  LECtAiNCHE.  Revue  Generale  de  Med.  Veterinaire.  1904,  p. 
49.  Abstract  of  article  in  Jour.  Comp.  Path,  and  Thera.  Vol.  XVII 
(1904),  p.  83. 

4.  IvODE  UND  Gruber.  Bakteriologische  vStudien  iiber  die  Aeti- 
ologie  einer  epidemischen  Erkrankung  der  Hiihner  in  Tirol  (1901). 
Cejitral-blatt  fi'ir  Bakt.     Bd.  XXX  (igoi),  S.  593. 

5.  Maggiora  UND  Vai^enTI.  Ueber  eine  Seuche  von  exuda- 
tivem  Typhus  bei  Hiihnern.  Zeit  fi'ir.  Hvgiene,  Bd.  XLII  (1903),  vS. 
1S5. 


CHAPTER  XIII. 


IMMUNITY  AND  PROTECTIVE  INOCULATION. 

^  440.  Immunity.  In  a  broad  sense,  inimunit}-  is 
"resistance  to  disease."  The  term,  however,  is  usually 
restricted  to  the  infectious  maladies  and  signifies  a  condition 
of  the  individual  which  enables  it  to  successfully  defend  itself 
against  the  invasion  of  its  tissues  and  organs  with  the  infecting 
microorganisms  or  to  resist  the  toxic  effect  of  the  invading 
organisms  should  they  gain  entrance  and  multiply  within  the 
body.  While  it  usually  applies  to  the  action  of  pathogenic 
bacteria,  the  protozoa  are  not  excluded.  It  will  be  seen  that 
immunity  is  only  relative  ;  it  is  neither  permanent  nor  con- 
stant but  varies  with  natural  and  artificial  conditions.  Accord- 
ing to  the  process  by  which  it  is  established  in  the  individual, 
immunity  is  recognized  as  natural  or  artificial. 

^441.  Natural  immunity.  The  term  natural  immunity 
has  been  applied  to  that  condition  or  ability  possessed  by  some 
races  or  species  of  animals  which  enables  them  to  resist  the 
natural  invasion  of  infecting  organisms  that  attack  other  varie- 
ties or  species  of  animals.  In  so  far  as  we  know,  it  is  a  con- 
dition inherent  in  the  very  nature  of  the  individual,  born  with 
it  and  transmitted  to  its  offspring. 

There  are  a  number  of  very  striking  examples  of  natural 
immunity.  The  Algerian  race  of  sheep  are  immune  to  natural 
infection  of  anthrax,  whereas  other  sheep  are  very  susceptible 
to  it.  The  equine  species  is  susceptible  to  glanders  but  the 
ruminants  are  immune.  Blackleg,  which  is  very  destructive 
to  cattle,  does  not  attack  horses,  the  carnivora  or  man.  There 
are,  however,  instances  where  there  seems  to  be  a  general 
immunity  but  where  individuals  are  occasionally  attacked. 
Thus,  it  is  not  usual  to  find  tuberculosis  in  the  carnivora,  but 


546  .IMMUNITY 

now  and  then  the  cat  or  dog  is  found  suffering  with  the  disease. 
While  it  must  be  admitted  that  all  species  may  be  infected 
with  tuberculosis  there  is  much  evidence  to  show  that  certain 
species  are  largely  immune  to  it. 

It  sometimes  happens  that  individuals  belonging  to  a  sus- 
ceptible species  resist  infection.  These  are  spoken  of  as  pos- 
sessing natural  immunity  ;  but  this  is  not  a  satisfactory 
explanation,  for  in  such  cases  it  is  practically  impossible  to 
state  whether  it  is  natural  or  acquired.  In  the  present 
state  of  our  knowledge  of  this  subject  it  seems  better  to 
allow  such  cases  to  remain  as  examples  of  individual  re- 
sistance. 

It  has  also  been  found  that  in  cases  of  marked  natural 
immunity  the  resistance  can  be  overcome  and  the  animal 
infected  by  changing  its  normal  physical  condition.  Thus 
fowls  that  are  naturally  immune  to  anthrax  are  said  to  be 
made  susceptible  to  its  bacteria  by  reducing  their  temperature 
by  immersing  them  in  cold  water.  Charrin  and  Roger  found 
that  fatigue  would  lessen  the  resistance  of  white  rats  to  the 
same  disease.  Gibier  found  that  frogs  kept  at  a  temperature 
of  37°  C.  were  susceptible  to  anthrax. 

It  has  been  stated  that  sewer  and  other  poisonous  gases 
predisposed  animals  to  infection.  Abbott  concluded,  after  a 
careful  experiment  of  exposing  rabbits  to  sewer  gas  and  gases 
of  putrid  meat,  that  they  did  not  lessen  the  resistance  of  the 
animals  to  infection.  Diet  and  drugs  have  been  reported  to 
have  been  successfully  used  in  reducing  the  resistance  to 
infection.  The  removal  of  the  spleen  has  been  thought  by 
some  experimenters  to  increase  the  susceptibility  but  others 
have  reported  different  results. 

Natural  immunity  usually  persists  under  ordinary  condi- 
tions throughout  life  and  in  that  respect  it  is  much  more  per- 
manent than  artificial  immunity. 

§  442.  Explanation  of  natural  immunity.  There  are 
a  number  of  explanations  of  this  phenomenon.  In  brief  they 
deal  with  the  supposed  actions  (r)  of  the  cells  of  the  body,  and 
(2)  of  the  serums  or  humors. 


ARTIFICIAL     IMMUNITY  547 

Those  who  seek  the  cause  for  this  condition  in  the  cells 
find  that  phagocytosis,  so  ably  described  and  demonstrated  by 
Metchnikoff,  is  the  source  of  the  individual  defence.  Those 
who  find  the  cause  in  the  humors  of  the  body  rely  upon  the 
germicidal  action  of  the  serum  itself  or  of  the  substances 
set  free  from  the  cells  that  are  present  in  the  liquids. 
Metchnikoff  seems  to  believe  that  the  microcytase  elaborated 
from  the  leucocytes  acts  as  a  solvent  directly  upon  the 
bacteria. 

The  lateral  side-chain  theory  of  Ehrlich  assumes  that  the 
cells  of  certain  animals  do  not  possess  the  necessary  combining 
molecules  (receptors)  with  which  the  haptophore  group  of 
atoms  of  the  toxin  molecule  could  unite,  thus  the  destructive 
action  of  the  toxin  upon  the  cell  is  prevented.  This  theory 
refers  immunity  to  the  resistance  of  the  animal  tissues  to  the 
toxin.  A  study  of  the  subject,  however,  shows  that  while 
many  interesting  facts  have  been  brought  to  light  a  satis- 
factory exposition  of  the  cause  of  natural  immunity  has  not 
appeared. 

§  443.  Artificial  immunity.  As  the  term  implies,  this 
is  immunity  brought  about  in  the  individual  after  birth.  The 
most  common  form  of  artificial  immunity  is  found  in  individ- 
uals that  have  survived  an  attack  of  an  infectious  disease. 
The  most  striking  examples  of  this  are  cases  of  recovery  from 
small  pox  and  yellow  fever  in  man  and  Texas  fever  in  cattle. 
All  of  the  exanthematous  diseases  leave  the  individual  with 
more  or  less  immunity.  In  .some  other  infectious  diseases  like 
tuberculosis  there  seems  to  be  very  little  if  any  increased 
power  of  resistance  imparted  to  a  patient  who  has  recovered 
from  the  first  attack.  In  such  acute  diseases  as  diphtheria, 
the  duration  of  the  immunity  resulting  from  a  natural  attack 
of  the  disease  is  somewhat  variable.  In  artificial  immunity 
there  is  great  variation  in  the  period  of  duration. 

The  fact  that  individuals  that  had  passed  through  certain 
diseases  were  rendered  immune  to  a  second  attack  led  Pasteur, 
Salmon,  Smith  and  others  to  inquire  into  methods  for  artifi- 
cially immunizing  animals  against  the  infectious  diseases  most 


548  IMMUNITY 

destructive  to  them.  The  first  experiments*  of  this  kind  on 
animals  appear  to  be  those  of  Pasteur,  who  found  that  inocu- 
lating animals  with  attenuated  virus  would  immunize  them 
against  inoculation  with  a  strong  virus  or  naturally  acquired 
infection.  He  prompth'  succeeded  with  swine  erysipelas, 
chicken  cholera,  and  anthrax.  Later  he  succeeded  with 
rabies.  Arloing,  Cornevin  and  Thomas,  and  Kitt  introduced 
a  successful  method  of  preventive  inoculation  with  attenuated 
virus  against  blackleg.  The  method  has  been  tried  with  a 
number  of  other  diseases  with  less  satisfactory  results. 

The  next  procedure  w^as  a  line  of  investigations  directed 
toward  the  production  of  immunity  by  the  use  of  toxins  or 
heated  cultures  of  the  bacteria.  The  first  of  these  was  an 
immunization  of  pigeons  against  hog  cholera  by  the  use  of 
heated  bouillon  cultures  of  the  bacillus  of  hog  cholera  by 
Salmon  and  Smith  in  iS86.  This  method  was  followed  with 
similar  results  by  Pasteur  with  chicken  cholera.  This  line  of 
investigation  led  eventually  to  the  immunizing  of  animals 
experimentally  with  the  toxins  or  heated  cultures  of  certain 
virulent  pathogenic  bacteria  such  as  diphtheria  and  tetanus. 

Another  method  that  has  been  extensively  tried  experi- 
mentally with  the  bacterial  diseases,  but  usually  without  suc- 
cess, is  the  use  of  non-lethal  doses  of  virulent  virus.  With 
certain  of  the  protozoan  diseases  this  method  is  more  successful, 
as  shown  by  the  excellent  results  that  are  being  reported  in 
immunizing  cattle  against  Texas  fever. 

It  has  been  found  that  the  blood  serum  of  animals  that 
are  immune  to  certain  bacterial  diseases  possesses  antitoxic 
properties  by   which   it  is  able  to  impart  immunity  to  healthy 


*This  principle  was  exemplified  centuries  before  in  the  far  East 
where  inoculation  with  small  pox  virus  (material  from  the  pustules) 
was  practiced  whenever  small  pox  occurred  naturally  in  a  very  mild 
form.  Lady  Mary  Wortly  Montague  is  said  to  have  introduced  this 
practice  into  Europe  about  17 18.  Later,  1796,  Jenner,  after  thirty  years 
of  labor,  introduced  the  practice  of  inoculating  human  subjects  with  the 
virus  of  cow  pox.  This  is  known  to-day  as  vaccination  and  the  vaccine 
is  prepared  at  the  present  time  from  calves.  In  1839,  Thiele  showed 
that  the  disease  known  as  cow  pox  was  small  pox  in  cattle. 


ARTIFICIAL    IMMUNITY  549 

susceptible  animals,  or  to  act  as  a  therapeutic  agent  for  those 
affected  with  the  same  disease.  Diphtheria  antitoxin  is  the 
most  striking  example. 

§  444.  Method  for  artificially  producing  immunity. 
The  present  knowledge  of  the  subject  shows  that  immunity 
may  be  produced  in  several  ways  other  than  by  causing  the 
individual  to  pass  through  an  attack  of  the  disease  caused  by 
natural  infection.  These  methods  may  be  summarized  as 
follows  : 

1.  By  inoculating  the  individual  with  a  non-lethal  do.se 
of  a  strong  virus.  This  is  practiced  in  immunizing  cattle 
against  Texas  fever,  sheep  pox  and  contagious  pleuro- 
pneumonia. 

2.  By  inoculating  the  individual  with  attenuated  virus. 
This  is  practical  in  anthrax,  blackleg,  chicken  cholera,  roiiget, 
and  rabies  and  bubonic  plague  in  man. 

3  By  inoculating  the  individual  with  a  vaccine  con.sist- 
ing  of  the  virus  of  the  di.sease  modified  by  continual  passage 
through  another  species  of  animal,  as  vaccine  for  small  pox. 

4.  By  the  injection  of  toxins.  In  practice  this  is  used 
for  immunizing  animals  such  as  horses  against  the  virus  ot 
the  diseases  for  the  purpose  of  procuring  antitoxin  from  their 
blood,  as  in  diphtheria  and  tetanus. 

5.  By  the  injection  of  antitoxins.  These  are  used  to 
immunize  animals  against  toxins,  and  children  against  natural 
infection,  as  in  diphtheria. 

^  445.  Active  and  passive  immunity.  In  methods 
producing  artificial  immunity,  most  of  them  require  the  intro- 
duction into  the  body  of  the  living  virus  or  the  injection  of  the 
products  (toxins  or  heated  cultures)  of  the  living  virus  in 
repeated  doses  and  constantly  increasing  quantities.  Immunity 
produced  by  any  of  these  procedures  or  by  the  recovery  from 
an  attack  of  an  infectious  disease  is  called  active  immunity. 
When  immunity  is  produced  by  the  injection  of  the  serum 
(antitoxin)  of  animals  already  immune  it  is  called  passive 
immunity. 


550  IMMUNITY 

Active  immunitj'  is  slow  in  its  appearance,  is  more  or  less 
dangerous  to  produce  and  is  always  attended  with  at  least 
some  discomfort.  It  varies  in  the  time  it  lasts  but  usually  it 
is  quite  persistent,  lasting  from  a  few  weeks  or  months  to 
several  3'ears.  Passive  immunity  is  quite  rapidly  produced,  is 
attended  with  little  or  no  danger  and  practically  no  discom- 
fort. It  is  very  limited  in  its  period  of  duration.  The  most 
extensive  use  of  passive  immunity  is  in  immunizing  children 
against  diphtheria.  It  is  not  employed  to  any  great  extent  in 
animal  diseases.  The  immunizing  of  horses  against  tetanus 
before  an  operation  is,  however,  practiced  bj-  many  operators. 

§  446.  Explanation  of  acquired  immunity.  A  number 
of  ingenious  explanations  have  been  offered  for  acquired 
immunity.  The  only  ones  that  have  withstood  the  test  ot 
their  objectors  are  those  of  Metchnikoff,  representing  the  cellu- 
lar theory,  and  of  Ehrlich,  representing  the  humoral  theory. 
The  results  from  different  lines  of  investigation  indicate  that 
the  factors  involved  in  securing  immunity  against  infectious 
diseases  are  multiple  in  number  and  varied  in  character.  As 
pointed  out  by  Meltzer  it  is  difficult  to  explain  immunity  as 
being  due  to  one  or  even  to  a  few  anti-bacterial  properties  of 
the  animal  body.  In  the  struggle  against  bacteria  the  defence 
of  the  body  is  carried  on  by  the  united  action  of  each  and 
every  resisting  influence.  However,  a  number  of  theories 
have  been  proposed. 

1.  The  exhaustion  theory.  This  theory  was  suggested  in 
1880  by  Pasteur,  who  thought  that  the  microorganisms  grow- 
ing in  the  body  used  up  some  substance  essential  to  their 
further  existence  and  died  out  leaving  the  body  unsuited  for 
future  occupation.  The  theory  could  not  apply  to  passive 
immunit}'^  produced  b}-  the  injection  of  antitoxin. 

2.  The  retentioii  theory.  This  was  proposed  by  Wernich 
and  Chauveau.  This  theory  is  based  on  the  fact  that  bacteria 
elaborate  some  metabolic  product  that  inhibits  their  further 
development  and  the  future  invasion  in  the  tissues  by  the  same 
species.     This  theory  is  illustrated  with   the   facts  shown  in 


THEORIES 


551 


the  cultivation  of  bacteria  in  artificial  media.  The  bacteria 
often  die  apparently  from  the  accumulation  of  metabolic  pro- 
ducts long  before  the  nutriment  is  exhausted.  After  these 
cultures  are  filtered  and  the  bacteria  present  are  removed, 
other  bacteria  of  the  same  species  will  not  grow  in  it.  This 
theory,  however,  does  not  explain  immunity  against  lysins, 
serpent's  venom  and  other  poisons. 

3.  The  phagocyfosis  theory.  Metchnikoff  has  supposed 
that  acquired  immunity  is  brought  about  because  of  the  action 
of  the  phagocytes  upon  the  invading  organisms.  He  has 
shown  that  in  cases  of  infection  with  the  Vibrio  Metchnikovi, 
the  phagocytes  of  unprotected  animals  do  not  take  up  the 
bacteria,  but  that  in  vaccinated  animals  they  do.  It  appears 
from  all  the  work  that  has  been  done  on  this  subject  that  the 
phagocytes  are  active  in  proportion  to  the  degree  of  immunitj' 
possessed  by  the  individual.  It  has  not  been  demonstrated, 
however,  whether  they  are  active  because  the  animal  is 
immune  and  the  bacteria  harmless  to  it,  or  whether  the  animal 
is  immune  because  the  phagocytes  are  destructive  to  the 
bacteria. 

4.  Tlie  Immoral  theory.  This  theory  is  based  on  the 
observations  of  Buchner,  Nuttall  and  others  that  blood  serum 
has  the  power  of  destroying  a  certain  number  of  bacteria  when 
introduced  into  it.  Nuttall  showed  in  addition  to  this  that  the 
bacteriolytic  power  ceased  if  the  blood  was  heated  to  55°  C. 
It  is  found,  however,  that  the  bacteriolytic  serums  occur  only 
in  cases  where  there  is  a  high  degree  of  forced  immunity, 
their  activity  being  in  proportion  to  the  degree  of  immunit}' 
obtained.  An  explanation  for  the  action  of  these  serums  upon 
bacteria  is  given  by  Khrlich  in  his  lateral-chain  theory. 

5.  Ehrlich' s  side-chain  theory.  According  to  Ehrlich,  in 
every  living  cell  there  must  exist  an  active  central  body  and  a 
number  of  other  chemical  groups  or  side  chains.  These  groups 
have  the  greater  variety  of  function,  especially  those  of  nutri- 
tion and  assimilation.  This  theory  teaches  that  immunity 
depends   upon   the   presence  or  absence  of  certain  substances 


552  IMMUNITY 

which  he  calls  receptors  or  lateral  chains  which  certain  of  the 
cells  possess.  These  receptors  are  concerned  in  the  normal 
nutrition  of  the  cells  and  have  affinities  for  various  complex 
albuminous  substances.  Among  these  substances  are  the 
molecules  of  the  toxin  produced  b}-  certain  bacteria  and  pos- 
sibh'  other  poisons.  Ever\'  toxin  has  affinities  described  as 
haptophorus  and  toxophorus,  that  is,  every  molecule  of  the 
toxin  is  composed  of  two  different  groups  of  atoms,  the  one 
the  toxophore  or  poisonous  group,  the  other  the  haptophore  or 
combining  group  of  atoms.  The  haptophorus  molecules  of 
the  toxin  combine  or  unite  with  the  receptors  of  those  cells  for 
which  they  have  special  affinity  and  through  the  haptophore 
group  the  toxophore  part  of  the  molecule  is  able  to  act  upon 
the  cell.  It  some  cases  the  cells  are  destroyed  and  in  others 
additional  receptors  seem  to  be  produced  because  of  the  stimu- 
lation. These  receptors  may  pass  out  of  the  cell  into  the 
serum,  where  they  act  as  free  receptors  or  immune  bodies  to 
lock  up  or  neutralize  the  toxin.  The  free  receptors  are  the 
active  part  of  the  antitoxin. 

Ehrlich  illustrated  his  theory  by  the  use  of  diagrammatic 
figures  to  represent  the  cell  throwing  off  "receptors,"  the  re- 
ceptors or  antitoxin  locking  up  or  neutralizing  the  toxin  and 
the  effect  of  the  anti- bodies  on  the  toxin  and  its  complement. 
The  accompanying  figures  are  taken  from  his  work. 

§  447-  Hemolysins.  Belfanti  and  Carbone,  in  1898, 
pointed  out  the  fact  that  if  horses  were  injected  with  the  red 
blood  cells  of  rabbits  the  serum  of  these  horses  would  be  more 
or  less  toxic  for  rabbits.  This  result  was  followed  with  some 
interesting  experiments  by  Bordet  in  which  he  showed  that 
the  blood  serum  of  guinea  pigs  that  had  been  injected  several 
times  with  from  three  to  five  cubic  centimeters  of  defibrianated 
rabbit's  blood  acquires  the  property  of  rapidly  dissolving  in  a 
te-st  tube  the  red  blood  cells  of  a  normal  rabbit's  blood.  The 
serum  of  an  untreated  healthy  guinea  pig  will  not  do  this. 
It  was  pointed  out  that  this  reaction  was  specific,  that  is,  the 
serum  of  animals  treated  with  rabbit's  blood  (specific  serum) 
dissolves  the  red  corpuscles  of  the  rabbit's  blood  only.      This 


HEMOLYSINS  553 


propertv  that  had  been  demonstrated  in  the  blood  serum  of 
guinea  pigs  treated  with  rabbit's  blood  was  shown  to  hold  for 
the  sera  of  other  species  of  animals  treated  with  the  blood 
cells  of  a  different  species.  Wassermann  has  formulated  this 
action  as  follows:  "The  serum  of  animals  species  A,  after 
these  have  been  injected  either  subcutaneously,  intrapento- 
neally,  or  intravenously  with  erythrocytes  of  species  B, 
acquires  an  increased  solvent  action  for  erythrocytes  of  species 
B,  and  only  for  this  species.  (There  are  a  few  exceptions  to 
this  general  rule).  We  call  this  hemolysis,  and  the  substances 
which  affect  the  solution  of  the  red  cells,  hemolysins  or  hemo- 
toxins." 

Bordet  has  been  able  to  show  that  the  solvent  power  of  the 
specific  hemolysins  depended  on  the  combined  action  of  two 
constituents  of  the  specific  serum.  Thus,  when  the  fresh 
hemolytic  serum  was  heated  for  a  half  hour  at  55°  C.  it  lost 
its  power.  If  to  this  inactive  serum  a  very  small  amount  of 
the  serum  of  a  normal  guinea  pig  was  added,  the  full  hemo- 
lytic power  was  restored  to  this  inactive  serum.  In  other 
words,  it  had  been  reactivated  by  this  addition.  This  experi- 
ment showed  that  the  hemolytic  action  of  the  specific  hemolytic 
.serum  depends  upon  two  substances  (i)  the  one  destroyed  by 
heating  to  55°  C.  and  which  is  contained  in  the  serum  of  the 
normal  untreated  animal  as  well  as  in  the  specific  hemolytic 
serum,  and  (2)  a  substance  that  is  able  to  withstand  heating 
to  55°  C.  and  which  is  contained  in  the  specific  serum  only. 

The  substance  which  is  destroyed  at  55°  C.  and  which 
exists  in  the  blood  of  the  untreated  animal  and  in  the  specific 
serum  constitutes  the  substances  designed  by  Buchner  as 
alexins.  It  is  the  substance  which  is  not  destroyed  by  heating 
to  55°  C.  .and  which  is  brought  about  by  the  action  of  the 
blood  of  one  species  upon  another  and  is  known  as  the  immune 
body,  or  as  termed  by  Buchner  substance  seJisibilatrice. 

§448.  Agglutinating  power  of  hemolytic  serum.  It 
has  been  found  in  the  experiments  by  Bordet  that  another 
property  was   increased  in   the   hemolytic  serum,  namely,  the 


554 


IMMUNITY 


power  of  clumping  red  blood  corpuscles.     This  clumping  or 
so-called  agglutination  of  the  red  cells  occurs  previous  to  their 


Fig.     122.       ,/,     Co)iip/e- 

metit ;     b,    iiitcruiediary 

body;     c,     receptor;     cf, 

part  of  the  cell. 


Fig.  123.  A  cell  ivith  different  kinds  of 
receptors;  b,  cell ;  c,  c  and  d,  different 
/cinds  of  receptors ;  a,  bodies  having  but 
one  haptophore  or  combinino;  group  of 


Fig.  124.  A  cell  shou'ing  the  separation 
of  the  receptors  or  antitoxin  and  the 
combination  of  toxin  with  free  anti- 
toxins;  c,  cell;  b,free  receptor;  a  toxin. 


Fig.  125.  A  draiving 
shoiving  the  action  of 
anti-complement;  a,  com- 
plement;  h,  intermedi- 
ary body  ;  c,  receptor  ;  d, 
cell ;  e,  anti-complement. 


I'KOTECTIVK    INOCl^LATION  555 

solution.  This  action  Bordet  considers  as  a  specific  one. 
Wasserniann  has  formulated  this  reaction  thus,  "  if  an  animal, 
species  A,  be  treated  with  blood  of  species  B,  the  serum 
derived  from  A  will  have  acquired  an  agglutinating  power 
which  differs  from  that  of  normal  serum  of  A  in  one  very  im- 
portant particular,  namely,  in  that  it  is  specifically  increased 
with  respect  to  the  red  cells  of  species  B  or  its  nearest  biologi- 
cal relative.  This  clumping  must  not  be  confounded  with 
rouleaux  formation  in  normal  blood." 

For  a  more  extended  discussion  of  the  subject  of  hemolysis 
and  for  cytolysis,  cytotoxins,  agglutinins  and  precipitins  the 
student  is  referred  to  the  special  literature  on  these  subjects. 

ij  449.  Protective  inoculation.  The  practical  applica- 
tion of  immunity  in  protective  inoculations  or  vaccination  has 
come  to  mean  the  establishment  of  partial  or  complete  im- 
munity in  the  individual  against  the  disease  in  question.  The 
vaccination  against  small  pox  introduced  by  Jenner  in  1796  is  a 
well  known  example  of  protective  inoculation.  Pasteur  found 
that  animals  inoculated  with  attenuated  cultures  of  anthrax 
and  chicken  cholera  bacteria  were  subsequently  immune  to 
their  respective  diseases.  From  this  there  has  developed 
many  procedures  for  establishing  both  active  and  passive 
immunity  against  a  number  of  diseases  of  animals.  The 
methods  that  are  now  in  use,  together  with  the  diseases 
against  which  they  are  employed,  may  be  summarized  as 
follows  : 

I.      Active  immunity. 

I .  The  injection  of  non-lethal  do.ses  of  the  virulent  virus. 
This  method  is  employed  most  extensively  in  immunizing 
cattle  against  Texas  fever  and  bovine  contagious  pleuro-pneu- 
monia.  It  is  used  in  France  to  immunize  against  sheep  pox 
(clavelization) . 

The  fact  that  su.sceptible  cattle  can  be  immunized  against 
Texas  fever  by  the  use  of  blood  from  immunized  animals  has 
been  demonstrated.  The  method  is  being  applied  with  suc- 
cess in   several   places   in   the   tick  infected  district.      It   is  a 


556  IMMUNITY 

practicable  method  but,  like  the  others,  it  should  not  be 
undertaken  without  a  realization  of  the  possible  unfavorable 
outcome. 

Since  the  i8th  century  there  has  been  practiced  in  France 
on  a  large  scale  the  artificial  immunization  of  sheep  by  the 
inoculation  of  the  virus  of  sheep  pox  just  as  the  variolization 
of  man  was  practiced  before  the  discovery  of  small  pox  vaccine. 
In  France,  the  law  requires  the  inoculation  (clavelization)  of 
flocks  in  which  sheep  pox  appears,  but  it  interdicts  the  prac- 
tice in  unattacked  flocks. 

2.  The  injection  of  animals  with  attenuated  cultures  of 
the  bacteria  of  the  disease  against  which  immunity  is  to  be 
established.  This  method  is  used  most  extensively  in 
anthrax,  rabies,  symptomatic  anthrax,  swine  erysipelas  and 
bovine  tuberculosis. 

The  practical  value  of  vaccination  for  rabies,  over  that  of 
most  other  diseases,  is  the  fact  that  it  is  effective  if  made  early 
in  the  period  of  incubation.  This  vaccination  taking  advant- 
age of  the  long  period  of  incubation  in  rabies,  constitutes  a 
form  or  type  of  handling  of  an  infectious  disease  intermediate 
between  protective  inoculation  and  a  therapeutic  method  of 
treatment. 

Many  efforts  have  been  made  to  procure  a  vaccine  for 
tuberculosis.  Pearson,  of  the  University  of  Pennsylvania,  and 
von  Behring  of  Marburg,  Germany,  have  done  the  most  work 
along  this  line.  A  number  of  other  w^orkers  have  reported 
results,  among  whom  de  Schweinitz,  Trudeau,  M'Fadyean 
and  Schiitz  may  be  mentioned. 

The  bovo-vaccine  of  von  Behring  consists  of  living  human 
tubercle  bacteria.  The  results  reported  by  von  Behring  and 
others  who  have  tried  his  vaccine  are,  for  the  greater  part, 
encouraging,  but  as  yet  the  method  is  in  the  experimental 
stage. 

II.  Passive  ivinmnity.  This  consists  of  a  temporary  im- 
munity produced  by  the  injection  of  the  blood  serum  of  an 
animal    that    has   been  immunized  to  the  disease.      It  is  em- 


PROTECTIVK    INOCULATION  557 

ployed    as    a    prophylactic    in    swine  erysipelas,   tetanus,  and 

diphtheria.  . 

The  use  of  the  tetanus  antitoxin  to  immunize  horses 
against  tetanus  before  subjecting  them  to  operations,  such  as 
castration,  or  after  receiving  punctures  of  the  skin  or  hoot 
("farrier's  puncture")  is  becoming  more  and  more  prevalent 
in  those  countries  and  localities  where  tetanus  is  common.  In 
France  it  seems  to  be  used  more  than  elsewhere.  The  extent 
to  which  it  is  employed  is  indicated  by  the  fact  that  m  1896 
there  were  sent  out  from  the  Pasteur  Institute  of  Pans  1,511 
bottles  of  10  cc.  each  of  tetanus  antitoxin  ;  in  1898  the  num- 
ber rose  to  24.950  bottles;  and  in  1900  it  exceeded  43.000. 
The  most  of  this  was  for  the  protection  of  injured  animals 
against  tetanus.  It  is  given  in  two  injections  from  10  to  12 
days  apart.  Large  animals  receive  20  cc.  but  small  ones  from 
6  to  10  cc.  at  each  injection. 

The  value  of  diphtheria  antitoxin  as  an  immunizing  agent 
against  diphtheria  in  children  is  a  welf- known  fact. 

III.  The  simultancoits  method.  This  consists  in  using  a 
strong  virus  together  with  an  immunizing  serum.  The  pro- 
cess is  of  comparatively  recent  date.  It  is  used  quite  exten- 
sively against  rinderpest,  anthrax,  and  in  rabies. 

In  case  of  rinderpest  the  animals  are  injected  with  a  pro- 
tective serum  simultaneously  with  the  virulent  blood.  The 
immune  serum  is  obtained  from  animals  that  have  recovered 
spontaneously  from  rinderpest  or  from  cattle  that  have  been 
immunized  by  bile  or  some  other  method.  The  serum  alone 
of  animals  that  have  recovered  spontaneously  possesses  very 
slight  protective  properties  unless  very  large  doses  are  given. 
Kolle  and  Turner  showed  that  if  animals  jiist  recovering  from 
an  attack  were  injected  with  large  quantities  of  the  blood 
coming  from  animals  suffering  with  a  fatal  attack,  the  pro- 
tective power  of  their  serum  was  markedly  increased.  This 
serum  may  be  kept  for  a  long  time  by  adding  a  small  quantity 
of  carbolic  acid. 

In  rabies  the  method    is   reported   to  be   most   successful. 
Its  essential  advantage  over  the  other  process  is  that  it  can  be 


558  IMMUNITY 

used  with  good  results  nnich  later  in  the  period  of  incubation. 
It  has  the  additional  practical  feature  that  the  number  of 
injections  is  minimized. 

In  anthrax  it  is  reported  to  be  giving  much  better  results 
than  the  double  inoculation  with  a  weak  and  stronger  vaccine 
as  followed  in  the  Pasteur  method. 

§  450.  Difficulties  and  dangers  to  be  considered  in 
vaccination.  The  results  of  the  efforts  that  have  been  put 
forth  during  the  last  twenty  years  to  obtain  control  over  the 
infectious  diseases  of  animals  show  that  with  the  victories 
there  have  been  many  failures.  Because  of  the  few  diseases 
for  which  vaccines  have  been  successful,  animal  owners  often 
look  upon  vaccination  as  a  safe  and  sure  means  of  heading  off 
all  infections.  Because  of  their  strong  faith  in  its  efficiency 
and  the  ease  of  its  application,  it  is  often  chosen  rather  than 
the  more  difficult  and  perhaps  immediately  more  expensive 
procedures  of  prevention  or  eradication.  For  a  few  diseases 
there  is  a  well-established  natural  basis  for  vaccination,  but 
with  others  such  a  foundation  does  not  appear  to  exist.  The 
reasons  for  occasional  failures  in  vaccination  are  not  difficult 
to  find.  The  analysis  of  the  principles  underlying  vaccination 
shows  that  it  means  the  establishing  of  immunity  by  the  intro- 
duction into  the  body  of  non-lethal  doses  of  virulent  virus  or 
the  use  of  a  virus  that  has  been  attenuated. 

It  is  not  always  eas}'  or  even  possible  to  know  the  exact 
degree  of  virulence  possessed  by  the  vaccine,  and  again  the 
resisting  forces  of  animals  vary  even  in  different  individuals  ot 
the  same  species.  If  the  virulence  is  too  great  or  the  resist- 
ance below  the  supposed  normal  the  vaccine  may  produce  dis- 
ease in  excess  of  the  amount  required  to  establish  immunity 
and  perhaps  it  may  kill  the  animals  it  was  intended  to  protect. 
This  is  a  result  that  has  been  experienced.  On  the  other  side, 
if  the  attenuation  of  the  virus  is  too  much,  or  the  natural  resist- 
ance unusually  high,  there  is  not  disease  (reaction)  enough 
produced  to  cause  any  immunity.  In  this  case  the  results  are 
negative.     In  cases  where  the  virulent  virus  is  used   in   small 


DANGERS    IN    VACCINATION  559 

doses,  accidents  have  happened  bj'  way  of  producing  a  fatal 
disease  instead  of  a  mild  attack  that  was  anticipated.  The 
difficulty  rests  in  the  procuring  of  a  vaccine  or  the  quantity  of 
a  virus  that  possesses  just  the  amount  of  disease-producing 
power  that  is  necessary  to  bring  about  immunity  and  no  more. 
This  is  a  balance  of  vital  forces  that  it  is  exceedingly  difficult 
to  strike. 

A  glance  at  the  diseases  for  which  active  immunity  has 
been  attained  will  show  that  they  are  acute  toxic  affections 
and  not  those  in  which  the  disease  consists  of  extensive  tissue 
destruction.  Toxic  immunity  has  been  attained  in  several 
disorders  but  a  bacterial  immunity  is  much  more  difficult  to 
acquire. 

As  vaccination  rests  upon  the  production  of  artificial 
immunity,  the  extent  to  which  it  can  be  applied  depends  upon 
the  efficiency  of  methods  to  produce  immunity  in  different 
diseases.  In  deciding  upon  the  action  to  be  taken  in  the  pres- 
ence of  an  infectious  disease,  the  selection  of  a  vaccine  should 
be  guided  by  the  fullest  knowledge  possible  of  the  nature  of 
the  disease  itself  and  the  extent  to  which  natural  and  acquired 
immunity  against  it  exists  or  is  made  possible. 

The  dangers  in  vaccination  as  applied  especially  to  animals 
at  large  may  be  summarized  as  follows  : 

1.  The  vaccine  may  be  too  much  attenuated,  resulting 
in  the  failure  to  establish  immunity. 

2.  The  vaccine  may  be  too  strong  (virulent)  so  that  it 
will  produce  more  disease  than  is  desired,  possibly  causing 
fatal  results. 

3.  The  attenuated  virus  of  which  the  vaccine  consists 
many  regain  its  virulence.  The  distribution  of  living  patho- 
genic microorganisms  among  animals  is  of  itself  not  to  be 
recommended.  They  may  be  the  starting  point  of  subsequent 
outbreaks. 

4.  In  using  non-lethal  doses  of  a  virulent  virus,  the  dan- 
ger of  producing  fatal  results  because  of  the  susceptiblity  of 
the  individual  treated  is  always  present. 

5.  In  the  simultaneous  method   the   danger   of  accident 


56o  IMMUNITY 

resulting  from  too  strong  a  virus,  too  weak  a  serum,  or  the 
high  resistance  or  unusual  susceptibility  of  the  individual  are 
possible  conditions  to  be  kept  in  mind. 

§  451.  Prevention,  The  prevention  of  the  specific  dis- 
eases of  animals,  when  considered  from  the  point  of  view  of 
etiology,  is  not  so  difficult  as  is  often  supposed.  Infectious 
diseases  are  simply  parasitisms.  If  the  infecting  organisms 
can  be  kept  away  from  animals  the  diseases  they  would  pro- 
duce cannot  appear,  and  if  the  individuals  already  suffering 
from  the  disease  are  properly  isolated,  their  stables  and  pens 
disinfected,  and  their  bodies  properly  destroyed  if  they  die, 
the  infecting  organisms  must  perish.  The  great  Pasteur  said, 
"  It  is  within  the  power  of  man  to  make  all  infectious  diseases 
disappear  from  the  world."  The  fact  that  the  bacteria  of 
these  diseases  are  parasites  restricts  their  breeding  places,  so  to 
speak,  to  the  animal  body.  If,  therefore,  the  channels 
through  which  these  microorganisms  escape  from  the  infected 
body  are  properly  guarded,  and  if  the  channels  through  which 
they  enter  the  healthy  body  are  intelligently  protected,  the 
spread  of  infectious  animal  diseases  will  be  minimized,  it 
not  entirely  prevented. 

Since  the  discovery  of  a  specific  etiology  the  life  history 
and  possibilities  of  the  virus  of  the  different  infectious  diseases 
have  been  diligently  studied  and  much  has  been  learned  con- 
cerning them.  The  result  is  that  frequently  by  taking  ad- 
vantage of  the  present  knowledge  of  the  infecting  organism, 
preventive  measures  may  be  taken  that  will  give  equally  as 
good  results  as  vaccine,  without  its  dangers,  and  often  with  as 
little  trouble  and  expense.  The  prevention  of  these  diseases 
is  well  illustrated  in  many  instances  where  owners  of  animals 
have  protected  their  herds  against  the  sources  of  infection 
when  surrounded  with  widespread  epizootics.  Whole  coun- 
tries have  been  kept  free  from  certain  maladies  by  enjoining 
the  same  methods,  as  shown  in  the  absence  of  rabies  in  Aus- 
tralia. This  was  accomplished  by  prohibiting  the  entrance  of 
dogs  until  after  they  had  been  quarantined  for  a  sufficient  time. 
The  eradication  of  infectious  diseases  by  holding  rigidly   and. 


PREVENTION  561 

simply  to  the  guarding  of  the  channels  of  dissemination  and 
infection  has  been  accomplished  a  number  of  times  on  a  large 
scale  as  instanced  by  the  eradication  of  contagious  pleuropneu- 
monia in  cattle  from  this  country  and  from  Great  Britain.  The 
elimination  of  foot  and  mouth  disease  from  New  England  is 
another  striking  illustration  of  active  decisive  efforts  in  this 
direction.  The  eradication  of  infectious  di.seases  from  individ- 
ual herds  is  being  accomplished  repeatedly  by  adhering  to  the 
same  methods.  The  Bang  method  of  handling  bovine  tuber- 
culosis, as  already  mentioned,  enables  one  to  protect  the  well 
animals  and  to  save  all  there  is  of  value  in  the  others. 

The  i-solation  of  the  well  from  the  sick  and  the  thorough 
disinfection  of  the  houses  and  yards  containing  the  sick  has 
resulted  in  stopping  many  outbreaks  of  disease.  This  is  fol- 
lowed very  generally  even  where  vaccination  and  serum  pre- 
vention treatment  are  resorted  to.  Several  times  in  the 
writer's  experience  success  in.  checking  the  spread  of  the 
di.sease  by  vaccination  was  not  attained  until  rigid  methods  of 
isolation  and  disinfection  were  carried  out.  Just  what  these 
methods  are  to  be  in  each  particular  case  will  be  indicated  by 
a  definite  knowledge  of  the  cause  and  the  nature  of  the  disease 
in  question. 

The  methods  for  immunization  that  give  the  greatest 
promise  in  aiding  in  the  solution  of  the  problem  of  the  control 
of  infectious  diseases  are  those  productive  of  a  passive  immunity. 
Although  these  are  temporary  in  duration  they  are  effective 
immediately  and  consequently  tend  to  save  individuals  when 
they  are  applied  in  the  period  of  incubation  or  before  a  possible 
exposure.  They  protect  the  animal  until  the  virus  can  be  elim- 
inated and  its  environment  made  safe. 

The  advantages  of  introducing  preventive  measures  are  : 

1.  The  tendency  to  eliminate  the  virus  of  the  disease 
if  it  is  present,  and  to  keep  it  away  if  it  has  not  already 
appeared. 

2.  The  animals  are  free  from  the  virus  and  there  is  no 
danger  of  their  subsequently  developing  lesions  due  to  the 
localization  of  the  attenuated  microorganisms. 


562  IMMUNITY 

3.  The  separating  of  the  well  animals  from  the  sick  ones 
and  from  the  infected  stables,  pens,  yards,  or  fields  is  not 
usually  an  expensive  procedure.  The  stables  and  yards  can 
be  disinfected  and  the  infected  fields  can  be  utilized  for  other 
purposes  until  the  virus  has  been  destroyed  by  its  own  limited 
life  cycle.  In  this  connection,  it  is  well  to  call  attention  to 
efforts  that  are  being  put  forth  to  eliminate  the  cattle  tick  from 
the  Southern  States  and  thus  prevent  Texas  fever. 

REFERENCES. 

1.  Ernst.     Modern  theories  of  Bacterial  Immunity.    Boston,  1903. 

2.  Metchnikoff.     Immunity  in  Infective  Diseases.     Cambridge. 
1905- 

3.  NuTTALL.     Blood   Immunity    and    Blood   Relationship.     Cam- 
bridge, 1904. 

4.  Sobernhf:im.     Deutsche  Med.  Wochenschrift.   1904,  No.  26,  S. 
27. 

5.  Sternberg.     Immunity,  Protective  Inoculations  in  Infectious 
Diseases  and  Serum-Therapy.     New  York,  1895. 

6.  Wassermann.     Immune   Sera,    Haemolysins,   Cytotoxins,  and 
Precipitins.     New  York,  1904. 

7.  Vaughn  and  Now.     Cellular  toxins  or  the  Chemical  Factors 
in  the  Causation  of  Disease. 


CHAPTER  XIV. 


DISINFECTION. 


^  452.  Disinfection.  By  disinfection  is  meant  the  de- 
struction of  infectious  disease-producing  organisms.  For  this 
purpose,  nature  has  provided  very  important  agents,  such  as 
sunhght  and  drying,  but  these  are  not  available  or  sufficient  to 
destroy  all  infecting  bacteria  in  all  infected  places  within  the 
necessary  time  limits.  To  supplement  these  natural  forces,  a 
large  number  of  chemical  substances  possessed  of  germicidal 
powers  have  been  brought  into  service.  If,  however,  the 
results  of  the  test  experiments  with  these  different  sub.stances 
are  reviewed,  one  is  impressed  with  the  discrepancies,  if  not 
contradictory  conclusions,  recorded  concerning  their  value.  In 
view  of  these  facts  the  practitioner  is  often  at  a  loss  to  know 
just  what  chemicals  to  use,  or  how  to  apply  them  under  different 
conditions  and  for  the  destruction  of  different  species  of  organ- 
isms. The  failure  resulting  from  the  many  efforts  to  disinfect 
stables,  pens,  kennels  and  yards  has  caused  much  skepticism 
concerning  the  efficiency  of  many  reported  disinfectants.  In 
order  to  rightly  understand  the  reason  for  the  differences  in 
results  of  the  test  experiments  or  the  lack  of  uniformity  in  the 
application  of  the  various  disinfecting  substances,  it  is  well  to 
take  into  account  certain  fundamental  facts. 

I .  The  bacteria  used  by  different  investigators  to  test  the 
efficiency  ot  certain  substances  have  not  been  the  same.  The 
vital  resistance  of  the  various  species  is  very  different.  The 
results  obtained  in  testing  disinfectants  on  the  spirillum  of 
Asiatic  cholera  or  the  bacterium  of  bubonic  plague  give  but 
little  information  relative  to  the  value  of  the  same  disinfectants 
when  used  for  the  destruction  of  the  bacteria  of  glanders, 
tuberculosis  or  hog  cholera.  Thus  the  difficulty  in  accepting 
the    results  of    many    of    the   older  experiments    is    that   the 


564  DISINFECTION 

organisms  were  used  which  are  very  unlike  those  for  which 
these  disinfectants  are  now  wanted.  The  practical  value  of 
the  more  recent  experiments  is  greater  because  they  have  more 
generally  dealt  with  species  of  bacteria  with  which  most  of  the 
work  of  disinfection  has  to  do. 

2.  The  power  of  resistance  of  the  same  species  of  bac- 
terium varies  greatly  under  different  conditions.  For  instance, 
Bear  found  that  a  freshly  inoculated  culture  of  the  bacterium 
of  diphtheria  was  destroyed  with  i  :50oo  of  nitrate  of  silver,  but 
that  a  twenty-four  hour  culture  required  1:1000  of  the  same 
agent  to  kill  it  in  the  same  space  of  time.  In  some  work  done 
by  Esmarch  he  made  use  of  anthrax  spores  from  seventeen 
different  sources.  They  were  destroyed  by  steam  at  212°  F. 
in  from  one  to  twelve  minutes  and  by  a  five  per  cent  solution 
of  carbolic  acid  in  from  two  to  forty-two  days. 

3.  The  medium  in  which  the  bacteria  exist  influences  the 
results  of  the  disinfectants.  The  bacterium  of  tuberculosis 
from  an  aqueous  suspension  dried  upon  threads  may  be  promptly 
destroyed  by  mercuric  chloride,  but  in  fresh,  purulent, 
tuberculous  discharges  it  cannot  be  trusted  to  destroy  them. 
Again  Behring  says  that  sporeless  anthrax  bacteria  in  water 
are  killed  by  corrosive  sublimate,  1:500,000;  in  bouillon,  by 
1 :40,ooo  ;  but  in  blood  .serum  not  with  certainty  with  a  solution 
of  1:2000.  Some  disinfectants  are  influenced  very  much  by 
the  character  of  the  material  which  contains  the  infectious 
organism,  while  other  disinfectants  are  influenced  to  a  com- 
paratively slight  degree.  The  experimental  work  which  does 
not  take  the  influence  of  the  media  upon  the  disinfectant  into 
account  is  not  of  much  practical  value  and  failures  are  to  be 
expected  in  the  work  of  the  disinfector  who  does  not  act  in 
accordance  with  this  fact. 

4.  The  temperature  under  which  the  disinfecting  agent 
acts  influences  ver}'  much  the  rapidity  and  the  certainty  of  its 
action.  Thus  Heider  found  that  anthrax  spores  that  survived 
the  action  of  a  five  per  cent  solution  of  carbolic  acid  thirty-six 
days  at  ordinary-  room  temperature,  were  killed  in  from  one  to 


PRACTICAL    DISINFECTION  565 

two  hours  at  131°  F.  Some  investigators  have  failed  testate 
the  temperature  under  which  their  disinfecting  experiments 
were  made. 

5.  In  many  of  the  results  the  inhibitory  action  of  the 
agent  in  question  has  been  mistaken  for  its  germicidal  action. 
After  the  bacteria  have  been  subjected  to  the  influence  of  a 
disinfectant  for  a  given  time,  though  not  killed,  their  vege- 
tating and  pathogenic  capabilities  may  be  modified  but  still 
able,  under  favorable  conditions,  to  return  to  their  former 
vigor. 

The  rules  and  recommendations  of  the  various  cattle  com- 
missions and  those  having  authority  in  methods  for  prevention 
of  infectious  disea.ses  of  animals  do  not  very  clearly  define  the 
procedures  best  adapted  to  the  various  places  and  conditions 
requiring  disinfection.  The  many  chemicals  possessed  of 
germicidal  powers  and  the  numerous  commercial  disinfectants, 
recommended  largely  from  the  results  of  certain  definite  tests, 
which  in  point  of  fact  may  be  of  no  value  in  determining  their 
efficiency  for  the  conditions  in  question,  render  further  inquiry 
into  the  best  methods  for  disinfecting  after  animal  diseases  a 
matter  of  much  scientific  interest  and  great  practical  value. 

S  453.  Conditions  to  be  taken  into  account  in  practical 
disinfection.  In  the  effort  to  destroy  the  microorganisms  in 
such  places  as  yards,  stables,  cattle  cars  and  the  like,  it  is  neces- 
sary to  consider  before  applying  a  disinfectant  the  following 
conditions  : 

1.  The  resistance  of  the  particular  organism  to  be  de- 
stroyed. 

2.  The  medium  or  material  in  which  it  exists. 

3.  The  nature  of  the  place  containing  the  organism  to  be 
destroyed. 

4.  The  chemical  action  of  the  material  surrounding  the 
microorganisms  on  the  disinfectant  itself. 

If  the  disinfection  is  for  anthrax  or  Texas  fever  (cattle 
tick)  a  more  powerful  substance  or  solution  must  be  employed 
than    would    be  required    in  disinfecting  for  the    bacteria  of 


566  DISINFECTION 

septicemia  hemorrhagica  or  hog-cholera.  If  the  infecting 
organisms  are  mixed  with  fecal  matter,  dirt  or  fodder,  the  prob- 
lem is  a  different  one  than  where  they  rest  on  a  comparatively 
clean  surface.  It  matters  again  whether  the  infecting  organisms 
are  in  the  soil  (on  surface),  on  a  stable  floor  that  is  tight  and 
hard  or  on  one  containing  cracks  of  various  sizes  and  made 
up  of  boards  more  or  less  shattered  or  destroyed,  thus  forming 
deep  crevices  for  the  hiding  away,  as  it  were,  of  the  specific 
organisms. 

In  the  disinfection  of  human  dwellings  the  fumigation 
with  formaldehyde  has  proven  to  be  one  of  the  cheapest  and 
ordinarily  the  most  efficient  procedures,  but  it  requires  a 
tightly  closed  room.  It  is  evident  that  such  a  method  cannot 
be  trusted  for  the  disinfection  of  most  barns,  stalls  or  .stables 
which  are  usually  large  compared  with  dwelling  rooms,  and 
what  is  of  far  more  importance,  they  are  too  open.  In  the 
disinfection  for  animal  diseases  the  agents  used  must  from  the 
nature  of  the  buildings  in  most  cases  be  applied  in  the  form  of 
a  solution. 

Jaeger's  investigations  brought  out  very  clearly  the  neces- 
sity of  adapting  the  disinfecting  agent  to  the  specific  kind  ot 
organism  to  be  destroyed.  For  instance,  while  brushing  the 
surface  with  a  i  :  3  milk  of  chloride  of  lime  destroyed  anthrax 
spores,  it  was  untrustworthy  as  a  disinfectant  for  the  bacteria 
of  tuberculosis  and  of  glanders.  For  the  destruction  of  the 
bacterium  of  tuberculosis  he  found  carbolic  acid  and  the  other 
coal-tar  phenols  very  efficient,  especially  when  acidulated  with 
.hj^drochloric  acid.  For  this  purpose  he  recommended  espe- 
cially Laplace's  4  per  cent  solution  of  crude  carbolic  acid  with 
two  per  cent  of  hydrochloric  acid.  In  the  hands  of  Jaeger, 
the  power  to  destroy  anthrax  spores  with  certainty  has  been 
shown  onl}^  by  solutions  of  carbolic  acid  and  the  thick  chloride 
of  lime  mixture. 

A  thick  milk  of  lime  applied  once  with  a  brush  Jaeger 
found  efficient  in  the  destruction  of  the  microorganisms  of 
chicken  cholera,  hog  cholera,  swine  erysipelas,  typhoid  fever, 
glanders,  anthrax  (without  spores)  and  Staphylococcus  pyogenes 
ajiretis. 


DISINFECTANTS  5^7 

Giaxa  in  a  similar  line  of  work  to  that  of  Jaeger's,  found 
that  in  the  disinfection  of  walls  even  a  five  per  cent  lime  wash 
acting  forty-eight  hours  failed  to  destroy  anthrax  spores,  the 
bacterium  of  tuberculosis  and  the  bacillus  of  tetanus. 

A  strong  solution  of  the  chloride  of  lime  may  be  classed 
as  one  of  the  rapidly  acting  disinfectants  for  most  bacteria,  but 
Jae-er's  report  of  its  failure  when  applied  to  the  infection  of 
tuberculosis  and  glanders  should  be  borne  in  mind.  For  the 
cleansino-  of  cattle  cars  Gruber  advises  scrubbing  them  out 
with  hot  water  or  washing  with  a  two  per  cent  solution  of  soda 
at  50°  C  ,  although  this  has  no  particular  disinfecting  power. 
If  the  cars  are  infected  he  sprays  with  a  5  to  10  per  cent  solu- 
tion of  formaldehyde. 

^  454.  Disinfectants  of  value  in  the  practical  disin- 
fection of  stables  and  pens.  For  disinfecting  pens,  stable 
floors  and  the  like  the  following  .solutions  have  been  recom- 
mended and  their  careful  and  intelligent  use  has  shown  them 
to  be  very  efficacious. 

I  Corrosive  sublimate  {^mercuric  ehloride),  i  ounee  in  8 
crallons  of  water  ^one-tenth  of  i  per  eent) .  The  water  should  be 
put  into  wooden  tubs  or  barrels  and  the  powdered  sublimate 
added  to  it  The  whole  must  be  allowed  to  stand  for  twenty- 
four  hours,  so  as  to  give  the  sublimate  an  opportunity  to 
become  entirely  dissolved.  Since  this  solution  is  poisonous 
it  should  be  kept  covered  and  well  guarded.  It  may  be  applied 
with  a  broom  or  mop  and  should  be  used  freely  on  all  wood- 
work Since  it  loses  its  virtue  in  proportion  to  the  amount 
of  dirt  present,  all  manure  and  other  dirt  should  be  first  removed 
before  applying  the  disinfectant.  The  manure  should  be  cov- 
ered with  lime  or  burned.  Its  very  poisonous  nature  for  man 
and  animals  renders  it  less  desirable  for  general  use  than  some 
other  solutions. 

o  Carbolic  acid.  A  5  percent  solution  of  carbolic  acid 
is  one  of  the  best  disinfectants  for  mangers,  feed  boxes  and 
fixed  watering  basins.  It  should  be  applied  in  quantity  suffi- 
cient to  thoroughly  wet  all  parts  and  soak  deep  into  the  cracks 
and  crevices  if  there  are  any. 


568  DISINFECTION 

3.  Chlormatedlime.  Five  ounces  of  chloride  of  lime  to  a 
gallon  of  water  (4  per  cent).  This  should  be  applied  in  the 
same  wa}^  as  the  corrosive  sublimate. 

4.  A  Diixiuj-e  of  crude  carbolic  and  sulphuric  acid.  The 
following  disinfectant  has  been  found  to  be  very  serviceable. 
It  is  not  poisonous,  but  quite  corrosive,  and  care  should  be 
taken  to  protect  the  eyes  and  hands  from  accidental  splashing  : 

Gallon. 

Crude  carbolic  acid 14 

Crude  sulphuric  acid y. 


These  two  substances  should  be  mixed  in  tubs  or  glass 
vessels.  The  sulphuric  acid  is  very  slowly  added  to  the  car- 
bolic acid.  During  the  mixing  a  large  amount  of  heat  is  de- 
veloped. The  disinfecting  power  of  the  mixture  is  heightened 
if  the  amount  of  heat  is  kept  down  by  placing  the  tub  or  glass 
demijohn  containing  the  carbolic  acid  in  cold  water  while  the 
sulphuric  acid  is  being  added.  The  resulting  mixture  is  added 
to  water  in  the  ratio  of  i  to  20.  One  gallon  of  mixed  acids 
will  thus  furnish  20  gallons  of  a  strong  disinfecting  solution, 
having  a  slightly  milky  appearance. 

5.  Formalin.  Formalin  is  being  highly  recommended  as 
a  disinfectant  when  used  in  a  5  per  cent  solution.  The  floors 
and  walls  should  be  thoroughly  wet  with  it. 

6.  Ordiyiary  slaked  lime.  Although  it  does  not  possess 
the  disinfecting  power  of  the  substances  given  above,  slaked 
lime  is  nevertheless  very  useful.  It  is  well  adapted  for  disin- 
fecting the  surface  of  yards  and  pens.  It  is  very  good  to  apply 
to  the  ceilings  and  walls  of  stables. 

There  are  a  number  of  other  substances  that  may  be  used, 
such  as  a  solution  of  blue  vitriol  or  creolin. 

In  disinfecting  stables  and  pens  all  litter  which  has  accu- 
mulated should  be  removed  before  applying  the  disinfectant. 
As  the  litter  itself  is  infected  it  should  be  disinfected  as  well  as 
the  stable  floor  and  walls.  The  most  efficient  method  for 
disinfecting  the  litter  is  fire.  The  practice  of  washing  the 
floors  and  ceiling  with  water   before  applying   the  disinfectant 


USK    OF    DISINFECTANTS  5^9 

has  in  most  instances  the  disadvantage  that  the  water  carries 
the  microorganisms  to  be  destroyed  into  cracks  and  possibly 
through  the  floor,  where  they  will  not  be  affected  by  the  later 
application  of  the  germicide.  It  is  deemed  safer  to  simply  use 
a  dry  cleaning,  avoiding  dust  as  much  as  possible,  and  to  burn 
the  sweepings  or  to  thoroughly  wet  them  with  a  strong  dis- 
infectant. The  disinfectant  is  then  applied  in  sufficient 
quantity  to  thoroughly  saturate  the  surfaces,  including  the 
adhering  particles  of  dirt.  The  solutions  available  for  stable 
disinfection  are  cheap  enough  to  admit  of  this  precaution. 

In  the  application  of  disinfectants  it  is  well  to  use  a  broom 
and  thoroughly  scrub  the  floor  and  lower  part  of  the  walls. 
This  is  necessarv  in  order  to  get  the  disinfectant  through  the 
dirt  and  into  the  crevices  of  the  floor.  The  disinfectants  can 
be  applied  to  the  ceilings  and  upper  parts  of  the  side  walls  with 
a  sprav  pump. 

It    is   often    desirable    to    disinfect    yards  where    infected 
animals  have  been  kept.     It  is  well  in  such  cases  to  carefully 
scrape  together  and  burn  the  litter,  after  which  the  surface  of 
the  soil  must  be  disinfected.     For  this  the  milk  of  lime  or  a 
very  liberal  coating  of  slaked  lime  has  been  recommended.    The 
burning  of  the  surface  such  as  can  be  done  by  covering  it  with 
a  layer  of  old  straw  and  burning,  is  a  more  certain   destroyer, 
especially    if    animal    parasities    are    to    be    eliminated.     The 
method  of  disinfecting  with  a  flame  as  described  by  Ferbusch 
in  1896,  and  recently  recommended  by  Stiles  for  disinfecting 
kennels',  pens  and  yards  offers  possibilities  not  found  in  other 
means.     The  procedure  consists  of  a   "Cyclone  burner  "    at- 
tached to  the  end  of  a   long   iron  tube   with   a  wooden  shield. 
This  is  connected  with  a  short  piece  of  hose  of  the  kind  made 
for  the  delivering  of  oil  attached  to  a  spray  pump.     A  tank  of 
suitable  .size  is  taken  and  paraffin  gas  oil  is  used.     The  spray 
of  oil  is  ignited,  giving  a  very  hot  and  eff-ective  flame,  which  is 
run  over  the  surface  to  be  disinfected.     The  flame  destroys  all 
living  things  on   the  surface.     This  method  seems  to  be  appli- 
cable to  the  disinfection  of  floors  and  stables  as  well  as  yards, 
when  the  conditions  are  permissible  and   when   tlie   flame  can 


570  DISINFECTION 

be  applied  with  the  necessary  care.  Experiments  are  being- 
made  to  determine  more  definiteh'  the  extent  to  which  this 
method  can  be  applied  with  safety. 

The  practical  use  of  disinfectants  is  a  matter  requiring 
much  attention  if  good  results  are  to  be  attained.  It  is  not 
wise  to  trust  the  disinfection  of  pens  and  stables  to  their  own- 
ers, unless  they  are  men  well  versed  in  the  knowledge  of  dis- 
infection. The  failure  to  properly  disinfect  stalls  and  stables 
is  frequently  the  secret  of  the  failure  to  stop  the  ravages  of 
infection. 

In  the  employment  of  commercial  disinfectants,  it  is 
necessary  also  to  know  the  destructive  value  of  the  solutions 
for  the  organism  to  be  destroyed.  There  are  many  so-called 
disinfectants  that,  in  the  strength  of  the  solutions  recom- 
mended, are  little  if  any  better  than  a  poor  antiseptic.  In  the 
destruction  of  pathogenic  microorganisms  it  is  important  to 
ever  keep  in  mind  that  the  disinfectant  must  be  able  to  kill 
the  organisms  in  the  condition  under  which  they  are  then 
existing. 

REFKRKNCKS. 

r.     Bracken.     Disinfection  and  disinfectants.      1901. 

2.  RiDEAL.     Disinfectants  and  disinfection.     London.     1895. 

3.  ROSENAU.     Disinfection  and  disinfectants.     1902. 

4.  SxitES.     The   disinfection  of  kennels,  pens  and  yards  by  fire. 
Bulletin  No.  35,  U.  S.  Bureau  of  Animal  Industry.     1902,     p.  15. 

5.  Young.      Notes  on  disinfectants  and  disinfection.     Reprinted 
from  the  loth  Report  of  tlie  State   Board  of  Health    of  Maine.     1898. 

(Contains  full  bibliography  on  disinfectants  and  results  of  experiments.) 


INDEX. 


A 

A  specific  infectious  disease —     3 

Actinobacillosis 317 

Characterization  317 

Differential  diagnosis, 320 

Etiology 3'7 

(Geographical  distribution  _3 17 

History 317 

Morbid  anatomy 319 

Prevention 320 

Symptoms 319 

Actinomycosis 299 

Characterization 299 

Differential  diagnosis 313 

Etiology 301 

Geographical  distribution  ,300 

History 299 

Infection^ 304 

Morbid  anatomy 307 

Sanitary  considerations 315 

Specific  treatment 314 

Symptoms 305 

Agglutinating  serum 553 

Ameba,  genus 377 

Anieba  dysenteriae 381 

Ameba  meleagridis 379 

Amebiasis 377 

Anthrax 129 

Animals  attacked 133 

Blood  in 141 

Channels  of  infection 133 

Characterization 129 

Differential  diagnosis 145 

Disposition  of  animals  dead 

of  anthrax 150 

Duration 144 

Etiology_    __.    131 

Geographical  distribution,  131 

History   129 

M'Fadyean's  stain 146 

Morbid  anatomy   139 

Pasteur's  vaccine  method__i47 

Period  of  incubation 133 

Prevention 149 

Prognosis 144 

Protective  inoculation 147 

Simultaneous  vaccine  meth- 
od   149 

Symptoms 135 


Apoplectiform     septicemia     in 

chickens, 57 

Characterization 57 

Differential  diagnosis 59 

Etiology 58 

Geographical  distribution.  58 

History 57 

Morbid  anatomy 58 

Prevention 59 

Symptoms 58 

Aspergillus  fumigattts 334 

glaucus 334 

Cultivation 333 

Asthenia  in  fowls  and  pigeons  243 

Characterization 243 

Etiology 243 

History 243 

Morbid  anatomy 244 

Symptoms 243 

Avian  tuberculosis 203 

Bacteria 205 

History  203 

Morbid  anatomy 206 

Symptoms 204 

B 

Bacillus,  genus 246 

of  blackleg 27S 

Bacillus  avisepticus 106 

hovisepticus 96 

clwlercc  suis 249,  260 

description  of 250 

cloacae 519 

coli  coininunis 29,  525 

enteritidis 291 

necrophorus .  289 

oedematis  maligni 286 

■    tetani 266,  267 

Bacteremia . 3 

Bacteria  causing   wound  infec- 
tion      8 

Bacterium,  discussion  of  genus.  69 

Bacterium  anthracis 131,  I45 

astheni(C 243 

of  Pieisz 236 

sanguinartum  1 14,1 15,122 
septiceniiae  hemorrha- 
gicae,  29,  70,  72,  87,  96,  113 
tuberculosis 175.   180 


572 


Cultivation  of 

Staining 

Bacterium  

tuberculosis  (avian)  _. 
Bacterium  of  swine  plague. 72, 

Of  fowl  cholera 

Bang's  method. 

Black  head   (see  infectious  en- 
tero-hepatitis). 

Black  leg 

Characterization 

DitTerential  diagnosis 

Duration 

Etiology 

Geographical  distribution. 

History 

^lorbid  anatomy 

Period  of  incubation 

Prevention 

Preventive  inoculation 

Symptoms 

Blastomycetes  infection 

Boophilus  annulatus 

Botryomycosis 


180 
213 


205 
260 
122 

224 


276    I 

276  I 
282 
282 
278    I 

277  [ 
27b 
280    I 
278 
283 
2S3 
279 
348    I 
355 

23    I 


Canine  malaria 372 

Characterization 372 

Etiology 373 

History 372 

Morbid  anatomy 374 

Symptoms 374 

Cellulitis  (infectious) 29 

Cerebro-spinal  meningitis 514 

Characterization 514 

Differential  diagnosis. 517 

Etiology.   514 

Morbid  anatomy 515 

Symptoms 515 

Channels  of  infection 5 

Chicken     cholera       (see      fowl 
cholera). 

Cladothrix  actinomyces 301 

Consumption  (see  tuberculosis) 
Contagious     pleuro-pneumonia 

in  cattle 441 

Characterization 

Differential  diagnosis. 

Eradication 

Etiology 

History 441 

In  the'U.  S. "442 

Morbid  anatomy 447 

Preventive  inoculation 452 

Symptoms --444 


441 
450 
452 
444 


Cornstalk  disease 517 

Characterization 517 

Differential  diagnosis .  522 

Etiology 520 

Geographical  distribution. 52a 

History 518 

Morbid  anatomy 521 

Symptoms 520 

Cow  pox.. _      533 

Lytodites  ntidus 212 

D 

Diarrhea  in  calves    (see   white 
scours). 

Diphtheria  in  calves  and  swine. 244 

Diphtheria  in  fowls 485 

Characterization 485 

Differential  diagnosis 494 

Etiology 486 

History 486 

Morbid  anatomy 490 

Prevention 495 

Relation    to    human    diph- 
theria   494 

vSymptoms 489 

Discomyces  equi 24 

Disinfectants 567 

Application  of 569 

Value  of 567 

Disinfection 563 

Practical 565 

Dog  distemper 506 

Characterization 506 

Differential  diagnosis 512 

Etiology 506 

Geographical   distribution. 506 

History 506 

Morbid  anatoni}^ 510 

Prevention 513 

Symptoms 507 

Dourine 410 

Characterization 410 

Differential  diagnosis 420 

Etiology 411 

History 411 

Morbid  anatomy 418 

Prevention ' 421 

Symptoms 415 

E 

Ehrlich's  side-chain  theory 552 

Epithelioma  contagiosum 539 

Characterization 539 


INDEX 


573 


Ktiolog}' --  -540   ! 

(Tcographical  distribution  .540    ! 

History 539    ', 

Morbid  anatomy 54i    1 

Symptoms 54^    1 

Epizootic  lymphangitis  342 

Characterization 342 

Differential  diagnosis 346 

Etiology 343 

History   342 

Morbid  anatomy 345    1 

Period  of  incubation 343 

Symptoms 344 

Equine  contagious  pleuro-pneu- 

monia 49 

Characterization 49    j 

Differential  diagnosis 56    1 

Duration 5^    I 

Etiology 50    I 

Geographical  distribution.  49   I 

History 49 

Morbid  anatomy 53 

Mortality 56 

Period  of  incubation ,  52 

Prevention 5^ 

Symptoms 52 

Equine  malaria , 3^9 

Characterization 3^9 

Differential  diagnosis 371 

Etiology 370 

Geographical  distribution_37o 

History 37° 

Morbid  anatomy 37^ 

Symptoms 37 1 

Etiology I 

F 

Farcy  (see  glanders). 

Farcy  in  cattle 346 

Fistulous  withers 3^ 

Foot  and  mouth  disease 454 

Characterization 454 

Differential  diagnosis .458 

Etiology 455 

Geographical  distribution. 454 

History 454 

Morbid  anatomy 457 

Period  of  incubation 455 

Prevention 45^ 

Symptoms  ._-   45^ 

Foot-rot  in  sheep 289 

Characterization 289 

Differential  diagnosis 291 

Etiologv 289 


History 289 

Morbid  anatomy 290 

Symptoms 290 

Forage  poisoning 5^7 

Fowl  cholera '05 

Blood  counts 109 

Characterization 105 

Differential  diagnosis. __.  .110 

Duration no 

Etiology 106 

Geographical  distribution.  106 

History 105 

Morbid  anatomy 107 

Period  of  incubation 106 

Prevention no 

Prognosis no 

Symptoms 106 

Fowl  pest 543 

Characterization  .__. 543 

Differential  diagnosis 544 

PZtiology - — 543 

Geographical  distribution_543 

History 543 

IVIorbid  anatomy 544 

Symptoms 544 

Fowrtyphoid "4 

Characterization 1 14 

Differential  diagnosis 120 

Etiology-   -.    115 

Geographical  distribution.!  14 

History n4 

Morbid  anatomy 116 

Prevention 122 

Symptoms US 

G 

Glanders — 151 

Agglutination  method ibb 

Animal  inoculation 165 

Characterization 151 

I  Dift'erential  diagnosis  .__-.  164 

Disposition      of      reacting 

horses '72 

Etiology ~—    153 

Geographical  distribution.  152 

Glanders  in  man 163 

History '5i 

Mallein 105 

Morbid  anatomy ^55 

Period  of  incubation I54 

Prevention ^53 

Serum  diagnosis 168 

Symptoms ^54 

Goose  septicemia ni 


574 


Characterization i  ii 

Differential  diagnosis 113 

Etiology III 

History m 

Morbid  anatomy 112 

Post-mortem  notes 113 

Prevention 113 

Symptoms i  [2 

Grouse  disease 283 

H 

Hemolysins 552 

Hemorrhagic      septicemia      in 

cattle 94 

Characterization 94 

Differential  diagnosis .103 

Duration 99 

Etiology 96 

Geographical  distribution.  96 

History 94 

Morbid  anatomy 99 

Period  of  incubation 97 

Prevention 103 

Prognosis 99 

Symptoms 97 

Hog  cholera 246 

Characterization 246 

Differential  diagnosis 259 

Duration 259 

Etiology 249 

Geographical  distribution. 248 

History 247 

Morbid  anatomy 254 

Period  of  incubation 253 

Prevention 262 

Prognosis  259 

Specific  treatment 264 

Symptoms 253 

Horse  pox 533 

I 

Ictero  hematuria  in  sheep 368 

Characterization 368 

Differential  diagnosis 369 

Etiology 368 

Geographical  distribution_368 

History 368 

Morbid  anatomy 369 

Symptoms 368 

Immunity 545 

Active  and  passive 549 

Artificial 547 

Explanation  of 550 


Natural 545 

Explanation  of 546 

Production  of 549 

Active 555 

Passive 556 

Simultaneous 557 

Infection 2 

Miscellaneous,  36,  244,  291,  346 
Umbilical 29 

Infectious  abortion 523 

Characterization 523 

Etiology 524 

History 523 

INIorbid  anatomy 525 

Prevention 528 

Infectious  cerebro-spinal  menin- 
gitis (seecerebro-spinal 
meningitis). 

Infectious  diseases 14 

Dissemination  of 14 

Prevention 560 

Infectious  entero-hepatitis 377 

Characterization 377 

Differential   diagnosis 389 

Etiology 379 

Geographical  distribution. 378 

History 377 

Morbid  anatomy 382 

Post-mortem  notes 388 

Prevention 390 

vSymptoms 3S1 

Infective  sarcomata  in  dogs 542 

Infectious  suppurative  cellulitis  29 

Influenza. 499 

Characterization 499 

Differential   diagnosis 505 

Etiology 501 

Geographical  distribution_50i 

History 500 

Morbid  anatomy 504 

Symptoms 504 

Ixodes  bovis 355 


Johne's  disease 230 

Characterization 230 

Differential  diagnosis 233 

Etiology 231 

History 230 

Morbid  anatomy 231 

Period  of  incubation 231 

Prevention 233 

Symptoms 231 


INDEX 


575 


Leeches 32i 

Characterization 321 

Ktiology 324 

Geographical  distribution. 324 

History 321 

Morbid  anatomy 3^5 

Treatment 332 

Leucoencephalitis 5 1 7 

Lockjaw  (see  tetanus). 

Lumpy  jaw  (see  actinomycosis). 

M 

Malaria,     bovine-     (see     Texas 
fever). 

Canine 372 

J/a/  de  caderas 423 

Characterization 423 

Differential  diagnosis 425 

Etiology 423 

Geographical  distribution_423 

History 423 

Mode  of  infection  ___    424 

Morbid  anatomy 424 

Symptoms  424 

Malignant  edema 286 

Characterization 286 

Differential  diagnosis 288 

Etiology 286 

History 2S6 

Morbid  anatomy 287 

Prevention 289 

Mallein 165 

MargavopHS  annulatus 355 

Mastitis,  infectious 32 

Mastitis,  streptococcic 60 

Characterization 60 

Differential  diagnosis 61 

Duration -  61 

Etiology     60 

Geographical  distribution.  60 

History 60 

Morbid  anatomy 61 

Period  of  incubation 61 

Symptoms 61 

Micrococcus,  discussion  of 63 

Micrococcus  ascoformans 24 

boti-yogenes 24 

capriiiiis 64 

laiict-olatus 73 

pyogenes  aureus,  8,  24,  63 
Migula's   classification  of  bac- 
teria  18,    19 


Musca  domestica 135 

Mycotic  stomatitis 347 

N 

Nagana 426 

Characterization 426 

Ditferential  diagnosis 427 

Etiology _--__— -426 

Geographical  distribution_426 

History 426 

Morl)id  anatomy 427 

Symptoms 426 

Navel-ill 25 

Negri  bodies 462,464,  482 

Normal  temperature  of  cattle,   218 
Effect  of  drinking  water  on.  221 


(Esoplniiio stoma  Columbianmn 

^ 212,  239 

Omphalophlebitis -— -   25 

Ovine  caseous  lymph  adenitis.234 

Characterization 234 

Differential  diagnosis 242 

Etiology 234 

Geographical  distribution  .234 

History  234 

Morbid  anatomy 238 

Symptoms 236 

P 

Pasteur's  anthrax  vaccine 147 

Pasteurelloses 69 

Pictou  disease ^3 

Piroplasnioses 349 

Piroplasma  in  horses 3^9 

Piroplasuia  bigeminnm 352 

canis 373 

equi 370 

ovis 368 

Pleuro  -  pneumonia  (see  con- 
tagious pleuro  -  pneu- 
monia). 

Pneumonomycosis 333 

Morbid  anatomy 337 

Species  of  fungi  — _ 333 

Pneumonomycosis  in  birds 341 

Poll  evil 31 

Protozoa -  -^ 349 

Protective  inoculation 555 


576 


Pseudo-tuberculosis(  see  Johne's 
disease ). 
In  sheep 234 

jyrosoma  bigeininiini 352 

Q 

Uuail  disease 293 

Ouarter-ill  (see  black  leg). 


Rabies 459 

Characterization 459 

Differential   diagnosis 477 

iJiinib 471 

Ktiology 462 

Furious 470 

Geographical  distribution. 461 

History 460 

Method  of  invasion 465 

Morbid  anatomy 472 

Period  of  incubation 467 

Prevention  and  treatment  .483 

Resistance  of  virus 466 

Symptoms 469 

Ray  fungus 301 

Rhodesian  redwater 352 

Rinderpest 430 

Characterization 431 

Differential  diagnosis 436 

Etiology 432 

Geographical  distribution. 43 1 

History 431 

Immunizing  cattle 439 

MorV)id  anatomy 434 

Prevention 437 

Symptoms 433 

Rinderseuche 94 


Saccharomycosis  farciminosus.343 

Sapremia 3 

Senecio  jacobea 13 

Septicemia 3 

Sheep  pox . 535 

Simultaneous  vaccine  method. 149 

Specific  infectious  disease 3,   n 

Cause  of  variation  in 15 

Differential  characters  of_.    il 

Dissemination  of l-_^  14 

Grouping  of '  16 


Spirillaceae 294 

Diseasesof  fowls  caused  by. 294 

vSpirillosis  of  cattle 295 

In  animals 297 

Disease  of  pigs 296 

Spirochaete  anserina 294 

vStrangles 44 

Characterization 44 

Differential  diagnosis 48 

Duration 47 

Etiology 45 

Geographical  distribution.  45 

History 44 

Morbid  anatoni}' 46 

Mortality 48 

Period  of  incubation 45 

Prevention 48 

Symptoms 45 

Strauss  method  of  inoculation.  55 

Streptococci 38 

Classification  of 40 

Diseases  due  to 33 

Distribution   in  nature 41 

General  discussion  of 38 

Pathogenesis  of 43 

Surra 400 

Characterization 400 

Differential  diagnosis 408 

p;tiology 401 

Geographical  distribution. 400 

History 400 

Means  of  transmission 402 

Morbifl  anatomy 404 

Period  of  incubation 402 

Prevention 409 

Report  of  Smith  and  Kin- 

youn 405 

Symptoms 403 

Swine  erysipelas --I23 

Characterization 123 

Differential  diagnosis 127 

Duration 127 

Pvtiology  ._ 124 

Geographical  distribution. 124 

History 123 

Morbid  anatomy 126 

Period  of  incubation 125 

Preventive  inoculation 128 

Prognosis 127 

vSymptoms 125 

Swine  fever  (see  hog  cholera). 

Swine  plague.    _. 71 

Autopsy  notes .  84 

Bacterium  of 74 

Characterization 71 


577 


Differential  diagnosis 86 

Etiology — -  72 

Geographical  distribution.  72 

History 7^ 

In  rabbits _^—  SS 

Modification  of,  in  rabbits,  60 

Morbid  anatomy 77 

Prevention 87 

Specific  treatment 88 

vSymptoms 76 

Symptomatic       anthrax       (see 
blackleg). 

T 

Tabanidae 135 

Takosis 63 

Characterization 63 

Differential  diagnosis 66 

Ktiology 64 

Geographical  distribution _  64 

History' 63 

Morbid  anatomy 65 

Prevention . 67 

Symptoms 64 

Tetanus 265 

Characterization 265 

Differential  diagnosis 273 

Duration 273 

Ktiology 266 

Geographical   distribution. 266 

History 266 

Mode  of  infection 268 

Morbid  anatomy 271 

Period  of  incubation 268 

Prevention 274 

Svmptoms 269 

Tetanus  antitoxin. 274 

Texas  fever 349 

Characterization 350 

Differential  diagnosis 363 

Etiology -  —  -352 

Geographical  distribution  350 

History . 350 

Immunizing  susceptible  cat- 
tle   364 

Infection 355 

:\Iorbid  anatomy 360 

Prevention 364 

Symptoms 35'^ 

Toxemia 3 

Trypanoplasma 391,  392 

Trypanosoma 391 

Classification 391 

Disappearance  after  deatli-395 


Distribution  in  the  body-__394 

History  .         529 

Historical  sketch 395 

Morphology 392 

Multiplication --393 

Staining 413 

Trj'/>a//osoma  Brucci,  394,  397,  426 

t-quhium 396.  397,  423 

e.qiiif)erdHm^.2>^(i,  397,  412 

Eviuisi 397,401 

Lcrcisi 39i-  397 

Tluilcrei 39^3 

Trypanosomata  and  their  hosts. 399 

Trypanosomiasis 39^ 

Differentiation 427 

Tse-tse  fly  disease  (see  Nagana). 

Tuberculin 215 

Application  of 217 

Preparation  of 215 

Tuberculosis . I75 

Characterization I75 

Control  of,  in  cattle 224 

Differential  diagnosis   211 

Animal  inoculation  —  214 
Microscopic  exam'tion,2 13 

Tuberculin  test 215 

Etiology iSo 

Extent    of,    in    cattle   and 

swine 17^ 

Generalized 197 

Geographical  distribution.  179 

History 176 

Localized 196 

Morbid  anatomy 188 

Prevention 223 

Symptoms 182 

Tubercle,  structure  of 191 

Vaccination 225 

Tuberculosis  in  fowls 203 

Symptoms  204 

Tuberculosis  in  swine 19^ 

Channels  of  infection 198 

Morbid  anatomy 200 

Symptoms^  __ 199 

Tuberculosisin  other  mammals  203 


Vaccination 55^ 

Dangers  of 55^ 

Variola  in  animals 529 

Characterization 529 

Etiology 533 

Geographical  distribution. 533 


578 


Symptoms 533 

Variola  in  horses 533 

in  cows 533 

in  goats 537 

in  sheep 535 

in  swine 53^ 

w 

White  scours 26 


Wildseuche 94 

Wound  infection 3,     6 

Bacteria S 

Morbid  anatomy 10 

Prevention jo 

z 

Zooglea  pulmonis  eqtii 24 


The  Pathology  and  Differential  Diagnosis 
of  Infectious  Diseases  of  Animals. 

By  Veranus  Alva  Moore,  B.S.,  M.D.,  Professor  of  Comparative  Path- 
ology, Bacteriology  and  Meat  Inspection,  New  York  State  Veterinary 
College,  Cornell  University,  Ithaca,  N.  Y.  With  an  introduction  by 
Daniel  Elmer  Salmon,  D.V.M.,  former  Chief  of  the  Bureau  of  Animal 
Industry,  United  States  Department  of  Agriculture. 


The  "Profession  will  gladly  welcome  this  new  book,  which  brings  the  subject 
right  up  to  the  present  state  of  the  wonderful  progress  made  in  the  study  of  infectious 
diseases.  *  *  The  book  deals  with  the  important  infectious  diseases  of  animals  that 
occur  in  this  country. — Am.  Vet.   Review. 

Dr.  Moore  has  rendered  an  invaluable  service  in  bringing  together  in  convenient 
book  form  a  lucid,  interesting  and  accurate  account  of  the  infectious  diseases  of  animals. 
— Am.  Med. 


Third  Edition.      Revised  and  Enlarged.      $4.00  net  Postpaid. 


Examination  of  the  Urine  of  the  Horse 
and  Man 

BY  PIERRE  A.  FISH,  D.Sc,  D.V.M. 

Simple  directions  are  given  for  performing  the  tests  necessary    to 
determine  the  normal  or  abnormal  conditions  of  the  urine. 

Price,  $1.50  net  postpaid. 

TAYLOR  &  CARPENTER 

VETERINARY  PUBLISHERS  AND  BOOKSELLERS 

ITHACA,   N.  Y. 


General    Surgery 


BY  DR.  MED.  EUGEN  FROHNER— Professor  In  the  Royal 
Veterinary  High  School  in  Berlin.  Authorized  Translation  from 
The  Third  Revised  Edition,  by  D.  HAMMOND  UDALL, 
B.S.A.,  D.V.M.,  Associate  Professor  of  Surgery  and  Obstetrics,  Ohio 
State  University,  Columbus,  Ohio. 

The  translation  of  Frohner's  General  Surgery  has  been  undertaken 
to  meet  the  need  of  an  English  text-book  on  the  subject.  This  text- 
book is  Vol.  II.  of  a  hand  book  of  seven  volumes  written  by  various 
authors  and  edited  by  the  late  Prof.  Joseph  Bayer,  of  Vienna  and  Prof. 
Eugen  Frohner  of  the  Berlin  Veterinary  School.  One  other  volume  of 
this  hand  book,  De  Bruin's  Obstetrics,  is  already  well  known  to  Eng- 
lish speaking  veterinarians. 

The  reputation  of  Prof.  Frohner  as  a  writer  of  text-books  is  too 
well  known  to  require  explanation.  This  translation  is  from  the  1 905 
edition  ;  the  subject  is  presented  in  a  scientific  manner ;  is  both  concise 
and  complete,  and  based  on  the  experience  of  many  years  of  carefully 
prepared  stastics  from  the  largest  clinic  of  its  kind  in  the  world. 

"  The  translator  has  earned  our  thanks  for  making  available  to  Non-German 
reading  \'eterinarians  one  of  the  best  of  the  numerous  works  on  General  Surgery. 
The  name  of  Professor  FrOhner  is  a  sufficient  guarantee  of  the  excellence  of  the  mat- 
ter and  the  convenience  of  its  arrangements.  The  work  contains  much  information 
not  to  be  found,  or  indifferently  treated  of,  in  others  of  the  same  class  and  some 
chapters,  notal)ly  those  on  tumour,  fractures  and  luxations,  are  admirably  written.  " 
THK  JOURNAL  OF  TROPICAL  VETKRINAKY  SCIKNCK, 

Calcutta. 

"  I  beg  to  thank  you  for  the  copy  of  Frohner's  General  \eterinary  Surgery  which 
I  received  from  you  a  short  time  ago.  It  is  an  excellent  work,  the  best  of  its  kind,  in 
my  opinion,  in  the  English  language. 

(Signed)       J.  J.  O'CONNOR,   M.   R.   C.  V.  S., 
Professor  of  vSurgery,  Royal  Veterinary  College  of  Ireland.  " 

"  The  original  work  of  Friihner  is  of  course  of  an  unusually  high  class  and  I  have 
found  your  translation  of  it  highly  satisfactory.  You  have  rendered  a  distinct  service 
to  veterinary  students  in  America  by  your  admirable  translation  of  this  work  which 
in  excellency  is  unsurpassed  in  Veterinary  literature. 

(Signed)       W.  L,.  WILUAMS, 
Professor  of  Surgery  New  York  State  A'eterinary   College,  Ithaca,   N.  Y.  " 

$3.00  net  postpaid 

TAYLOR  &  CARPENTER 

VETERINARY  PUBLISHERS  AND  BOOKSELLERS 

ITHACA,  N.  Y. 


B 


Y  PIERRE   A.  FISH,  D.Sc,   D.V.M.      Professor  of  Veterinary 
Physiology  and  Pharmacology,  New  York  State  Veterinary  Col- 
■,  Cornell  University,  Ithaca,  N.  Y. 


Veterinary  Doses  and  Prescription  Writing 

A  full  list  of  drugs  with  their  doses  for  the  different  domestic  ani- 
mals. Therapeutic  terms  and  a  list  of  terminations  of  medical  terms 
applicable  to  Veterinary  medicine.  Prescription  writing  is  discussed  in 
some  detail,  with  illustrative  prescriptions.  Thermometric  equivalents. 
Weights  and  measures.  Latin  words  and  phrases  used  in  prescription 
writing.  Incompatability.  Poisons  and  their  antidotes.  Classification 
of  medicines  according  to  their  physiologic  actions.  Pages  for  selected 
prescriptions. 

Red  Leather  Flexible  Covers,  1 60  pages.  Third  Revised  and 
Enlarged  Edition  $1.50  net  Postpaid. 

*     *     *     A  small  volume  which  will  be  of  indispensable  value  to  practitioners 
and  students.      ■■      *  It  will  return  the  investment  with  interest  every   other   day. — 

American  Veterinary  Review. 


Elementary  Exercises  in  Materia  Medica 
and  Pharmacy 

BY  PIERRE  A.  FISH,   D.Sc,  D.V.M. 

A  laboratory  manual  treating  of  the  more  commonly  used  inorganic 
and  organic  drugs.  Charts  are  included,  upon  which  are  to  be  plotted 
physiologic  action  of  many  of  the  drugs.  The  pharmaceutical  section 
includes  examples  of  the  different  preparations  in  the  U.  S.  Pharmacopoeia. 

Second  Edition.      Revised  and  Enlarged.      $1.50  net  Postpaid. 

There  are  features  in  this  book  which  betoken  a  grateful  advance  in  the  medical 
and  pharmaceutical  professions.  We  congratulate  Prof.  Fish  on  his  work. — Alkalodial 
Clinic. 

TAYLOR  &  CARPENTER 

VETERINARY  PUBLISHERS  AND  BOOKSELLERS 

ITHACA,  N.  Y. 


Exercises  in  Physiology 

BY  PIERRE  A.  FISH,  D.Sc,  D.V.M. 

A  laboratory  manual.       Part    I,    Chemical    Physiology.       Part   II, 
Experimental  Physiology. 

Second  Edition.     Revised  and  Enlarged.      $1.50  net  Postpaid. 

The  work  is  modern.  Its  directions  are  admirably  concise  and  clear.  It  will 
aid  teachers  as  well  as  students.— /our.  of  Applied  Microscopy  and  Laboratory 
Methods. 


Veterinary  Medicine 


By  Professor  James  Law,  F.R.C.V.S. 

Director  N.  Y.  S.  Veterinary  College,  Ithaca,  N.  Y. 

VOL.  1.  General  Pathology :  Diseases  of  the  Respiratory  and  Circu- 
latory Organs,  pp.  566.  8  vo.  2nd  Ed.  Revised  and  en- 
larged.     Price  $4.00. 

VOL.  11.  Diseases  of  Digestive  Organs,  Liver,  Pancreas  and  Spleen. 
pp.595.    8  vo.    2nd  Ed.    Revised  and  enlarged.    Price  $4.00. 

VOL.  111.  Diseases  of  Urinary  and  Generative  Organs,  Skin,  Eye  and 
Nervous  System,  pp.  61  1.  8  vo.  2nd  Ed.  Revised  and 
enlarged.     Price,  $4.00. 

VOL.  IV.  Infectious  Diseases,  Sanitary  Science  and  Police,  pp.  675. 
8  vo.      2nd  Ed.  in  Press.      Price,  $4.00. 

VOL.   V.      Parasites    and    Parasitism.       1st    Ed.      pp.    532.      8    vo- 
Price,  $4.00. 
Destined  to  become  a  standard  authority. — Am.    Vet.  Review. 
No  better  work  of  reference  could  be. —  Veterinary  Record. 

Of  Professor  Law's  latest  volume  (IV),  we  can  speak  in  terms  of  warm  praise. 
With  Its  companion  volumes,  will  form  a  valuable  addition  to  the  literature  of  veterinary 
medicine. — Jour,  of  Comp.  Path,  and  Thera. 

Published  by  the  author.     Sent,  express  prepaid,   on  receipt  of  price. 

TAYLOR  &  CARPENTER 

VETERINARY  PUBLISHERS  AND  BOOKSELLERS 

ITHACA,  N.  Y. 


THIS  BOOK  IS  DUE  ON  THE  LAST  DATE 
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OCT  2     193-. 

LD  21-100m-8,'34 

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